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Fontana, Roberto (2016) Alzheimer's disease mouse models based on presenilin-2 N141I: an in vivo study of spontaneous electrical activity by means of hippocampal extracellular recordings. [Tesi di dottorato]

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Abstract (inglese)

Alzheimer's disease (AD) is a neurodegenerative pathology that affects an increasing number of elderly people. It is characterized by progressive impairment in cognition and memory and it is the most frequent cause of dementia, being responsible for 60 to 70 % of the cases over 65 years (World Health Organization, 2015).
The major neuropathological hallmarks of the disease are the deposition of neurofibrillary tangles and senile plaques, primarily in hippocampus, entorhinal cortex and neocortex, and a widespread neuronal loss (Hardy and Selkoe 2002).
AD is divided in sporadic and familial (FAD) forms. FAD is caused by highly penetrating mutations in three genes involved in amyloid-ß (Aß) metabolism: the Aß precursor protein (APP), the presenilin1 (PSEN1) and the presenilin2 (PSEN2) (Bertram and Tanzi 2011).
The earliest pathological changes are believed to take place in the hippocampal formation and entorhinal cortex (Squire, Stark, Clark 2004). These regions are part of the medial temporal lobe and are fundamental for the encoding of new memories as well as for the fixation of recent ones. Moreover, they are among the first targets of the pathology in terms of tissue abnormalities and neuro-physiological alterations; these latter well correlate with memory deficits, being early symptoms of the disease (Sperling, Mormino, Johnson 2014; Squire, Stark, Clark 2004).
The most prominent network activity patterns in the hippocampus are field potential oscillations in the theta (4 - 12 Hz) and gamma (30 - 100 Hz) frequency bands. Theta and gamma oscillations are considered to play a pivotal role in memory as their properties, namely the amplitude, the frequency and the degree of their coupling, change during memory processes; moreover, they are predictive of learning performance (Lisman and Jensen 2013).
Several brain oscillations have been shown to interact, a phenomenon known as cross-frequency coupling (CFC) (Canolty and Knight 2010). One particular type of interaction consists in the phase of a slower oscillation modulating the amplitude of a faster one, hence the name phase-amplitude CFC (PAC). The PAC of theta on gamma oscillations in the hippocampus has drawn a growing interest since it has proven to be a physiological feature remarkably suited for predicting memory performance (Axmacher et al. 2010; Tort et al. 2009). Most notably, theta-gamma decoupling in the hippocampus impairs memory performance (Shirvalkar, Rapp, Shapiro 2010).
Further, a characteristic of brain electrophysiological signals is the "1/f" behavior of the frequency-domain power spectrum, meaning that the amplitude of each frequency component decays as a function of the frequency. Along with other features, the steepness of the decay has recently been shown to be informative about network activity.
At present, there are no therapies to reliably revert or stop AD. A biomarker (or a combination of biomarkers) for a non-invasive early diagnosis of the pathology "i.e. before the emergence of the cognitive deficits" would improve the efficacy of current and future strategies to contrast the progression of the disease (Sperling and Johnson 2013a).
Notwithstanding, FAD mutations of presenilin 1 (PS1) and, in particular of presenilin 2 (PS2) were shown to determine calcium (Ca2+) homeostasis impairment, a common feature in AD (Zampese et al. 2011a). In particular, Ca2+ defects due to PS2-N141I appear to occur independently of Aß load (Kipanyula et al. 2012). However, at the brain network level, outcomes due to the mutant PS2 have not been explored.
The aims of this work were (i) the assessment of the effects of the PS2-N141I FAD mutation on the above-mentioned aspects of the hippocampal network activity and (ii) the identification of novel potential electrophysiological markers of the preclinical phase of AD. To these ends, we employed two FAD mouse models, PS2.30H and B6.152H, which express the human PS2-N141I mutation respectively alone or in combination with the human APP Swedish mutation (Ozmen et al. 2009; Richards et al. 2003).
We investigated the local field potential (LFP) signal in the dentate gyrus (DG) region of the hippocampus in the condition of urethane anesthesia. Through the exploitation of frequency and time-frequency methods, we extracted several signal features, including amplitude, spectral steepness and theta-higher frequencies PAC. The temporal evolution of these features was assessed by investigating three age points, namely 3, 6 and 12 months. Additionally, we characterized our transgenic lines for three known molecular and histological biomarker of the disease. We quantified the degree of Aß42 load at each time point while the presence of amyloid plaques and astrogliosis was addressed at 3 and 6 months of age.
At 6 months of age, we report a significant power increase of slow-gamma (SG, 25 - 40 Hz) and high-gamma (HG, 40 - 90 Hz) oscillations in the PS2.30H line and of beta (10 - 25 Hz) and SG oscillations in the B6.152H line. Gamma oscillations and, more generally, a broadband power increase are generated by local network activity and are linked to active computation (Buzsaki and Wang 2012). The enhancement of beta and gamma power that we observe in our models likely reflects neuronal hyperactivity, consistently with similar observations in both sporadic and familial AD as well as in several AD mouse models (Stargardt, Swaab, Bossers 2015). In our mouse lines, this is the first time that the condition of neural network hyperactivity is described, although in vitro neuronal Ca2+ hyperexcitability was previously reported (Kipanyula et al. 2012). In B6.152H mice, hyperactivity was timed with the appearance of amyloid plaques and astrogliosis, whereas in PS2.30H mice no molecular or histological biomarker significantly differed from the wt (wild-type) line at any investigated age. The observed hyperactivity is possibly due to the expression of the mutant PS2, rather than to the Aß load which we probed to be profoundly different in the two AD mouse lines.
Only in the B6.152H line we found a more complex pattern of alterations. In addition to the broadband power increase, we report an enhancement of theta-beta and -SG PAC in this line at 6 months. Moreover, B6.152H mice displayed a steeper power spectrum slope compared to wt mice at 3 and 6 months of age. Both the overcoupling and the steeper spectral slope are ascribable to a condition of neuronal hyper-synchronicity, though with notable differences (Voytek and Knight 2015). Remarkably, we found that the difference between B6.152H and wt mice in terms of steepness was strongest at 3 months of age and diminished with ageing. Therefore, although further investigation will be required to validate this finding, hippocampal network hyper-synchronicity appears to be a promising early marker of the disease, at least in the context of a high Aß load.

Abstract (italiano)

La malattia di Alzheimer (AD, Alzheimer's disease) è una patologia neurodegenerativa che colpisce un numero crescente di anziani. E' caratterizzata da progressivo indebolimento delle funzioni cognitive e della memoria ed è la causa pi๠comune di demenza, essendo responsabile del 60 - 70 % dei casi al di sopra dei 65 anni (World Health Organization, 2015).
I principali elementi neuropatologici caratteristici della malattia sono la deposizione di ammassi neurofibrillari e placche senili, in primis in ippocampo, corteccia entorinale e neocorteccia, e una diffusa perdita di neuroni.
L'AD si divide nelle forme sporadica e familiare (FAD, familial AD). La FAD è causata da mutazioni ad alto grado di penetranza a carico di tre geni coinvolti nel metabolismo della ß-amiloide (Aß, amyloid-ß): Aß precursor protein (APP), presenilin1 (PSEN1) e presenilin2 (PSEN2) (Bertram and Tanzi 2011).
Si ritiene che i primi cambiamenti patologici abbiano luogo nella formazione ippocampale e nella corteccia entorinale (Squire, Stark, Clark 2004). Queste regioni fanno parte del lobo medio-temporale e sono fondamentali per la codifica di nuovi ricordi, così come per la fissazione di quelli recenti. Esse, inoltre, rientrano tra i primi bersagli della malattia in termini di alterazioni istologiche e neuro-fisiologiche; queste ultime correlano bene con i deficit mnemonici e sono considerate sintomi precoci della malattia (Sperling, Mormino, Johnson 2014; Squire, Stark, Clark 2004).
In ippocampo l'attività di network pi๠evidente è data dalle oscillazioni dei field potentials nelle bande di frequenza theta (4 - 12 Hz) e gamma (30 - 100 Hz). Si ritiene che le oscillazioni theta e gamma giochino un ruolo centrale nei processi di memoria, in quanto le loro proprietà , ovvero l'ampiezza, la frequenza e il loro grado di accoppiamento, cambiano durante i processi mnemonici; inoltre, esse sono predittive della prestazione di apprendimento (Lisman and Jensen 2013).
E' dimostrato che molte oscillazioni cerebrali interagiscono tra di loro, un fenomeno noto come cross-frequency coupling (CFC) (Canolty and Knight 2010). Una particolare tipologia di interazione consiste nella modulazione esercitata dalla fase di un'oscillazione pi๠lenta sull'ampiezza di un'altra pi๠veloce, da cui il nome CFC fase-ampiezza (PAC, phase-amplitude CFC). In ippocampo, il PAC delle oscillazioni theta sulle gamma ha attratto un crescente interesse, in virt๠del fatto che ha dato prova di essere un aspetto fisiologico notevolmente adeguato per predire la prestazione mnemonica (Axmacher et al. 2010; Tort et al. 2009). In particolare, la perdita di coupling in ippocampo compromette il processo di apprendimento (Shirvalkar, Rapp, Shapiro 2010).
Inoltre, una caratteristica dei segnali elettrofisiologici cerebrali è il comportamento '1/f' dello spettro di potenza nel dominio della frequenza, nel senso che l'ampiezza di ogni componente in frequenza decade in funzione della frequenza. Assieme ad altre caratteristiche, la rapidità di decadimento dello spettro di potenza (steepness), misurata come pendenza della funzione in una rappresentazione semilogaritmica, si è rivelata particolarmente informativa dell'attività di network.
Allo stato attuale, non esistono terapie efficaci per arrestare o far regredire l'AD. Un marcatore (o una combinazione di marcatori) per una diagnosi precoce non invasiva della patologia "cioè prima della comparsa dei deficit cognitivi" migliorerebbe l'efficacia delle strategie attuali e future per contrastare la progressione della malattia (Sperling and Johnson 2013a).
Inoltre, è stato provato che le mutazioni FAD della presenilina 1 (PS1) e della presenilina 2 (PS2) sono in grado di alterare l'omeostasi del calcio (Ca2+) intracellulare, una caratteristica comune nell'AD (Zampese et al. 2011a). Recentemente, è stato poi dimostrato che gli effetti della PS2-N141I sull'omeostasi del Ca2+ sono precoci ed indipendenti dai livelli di Aß (Kipanyula et al. 2012; Zampese et al. 2011a) Tuttavia, gli effetti della PS2 mutata a livello del network cerebrale non sono stati ancora esplorati.
Gli obiettivi di questo lavoro erano (i) la valutazione degli effetti della mutazione FAD PS2-N141I sugli aspetti sopracitati dell'attività di rete ippocampale e (ii) l'identificazione di nuovi potenziali marcatori elettrofisiologici della fase preclinica dell'AD. A tal fine, abbiamo impiegato due modelli murini di FAD, PS2.30H e B6.152H, che esprimono la mutazione umana PS2-N141I, rispettivamente da sola o in combinazione con la mutazione Svedese dell'APP umana (Ozmen et al. 2009; Richards et al. 2003).
Abbiamo studiato il local field potential (LFP) nella regione del giro dentato (DG, dentate gyrus) in ippocampo, nella condizione di anestesia con uretano. Attraverso metodi di analisi in frequenza e tempo-frequenza, abbiamo estratto diverse caratteristiche del segnale, tra cui l'ampiezza, la pendenza spettrale e il PAC tra oscillazioni theta e a frequenze maggiori. L'evoluzione temporale di queste caratteristiche è stata valutata analizzando tre età , ovvero 3, 6 e 12 mesi. Inoltre, abbiamo caratterizzato le nostre linee transgeniche per tre noti marker molecolari ed istologici della malattia. Abbiamo quantificato il livello di Aß42 ad ogni punto temporale, mentre la presenza di placche amiloidi e di astrogliosi è stata investigata a 3 e 6 mesi di età .
A 6 mesi di età , riportiamo un significativo aumento della potenza delle oscillazioni slow-gamma (SG, 25 - 40 Hz) e high-gamma (HG, 40 - 90 Hz) nella linea PS2.30H e delle oscillazioni beta (10 - 25 Hz) e SG nella linea B6.152H. Le oscillazioni gamma e, pi๠in generale, un aumento di potenza ad ampio spettro, sono generate dall'attività del network locale e riflettono processi di computazione attiva (Buzsaki and Wang 2012). L'aumento della potenza nelle oscillazioni beta e gamma che osserviamo nei nostri modelli riflette, probabilmente, iperattività neuronale, coerentemente con osservazioni simili riportate nelle forme sia sporadica che familiare dell'AD, così come in diversi modelli murini di AD (Stargardt, Swaab, Bossers 2015). Nelle nostre linee, questa è la prima volta che la condizione di iperattività neurale di network è descritta, anche se in vitro era stata precedentemente riportata ipereccitabilità neuronale basata sul Ca2+ (Kipanyula et al. 2012). Nei topi B6.152H, l'iperattività coincide temporalmente con la comparsa delle placche amiloidi e dell'astrogliosi, mentre nei topi PS2.30H nessun marcatore molecolare o istologico risulta significativamente diverso dalla linea wt (wild-type) a qualunque delle età indagate. L'iperattività osservata è probabilmente dovuta all'espressione della PS2 mutata, piuttosto che al livello di Aß, il quale si è rivelato essere profondamente diverso nelle nostre due linee modello dell'AD.
Solo nella linea B6.152H abbiamo trovato un pattern pi๠complesso di alterazioni. Oltre all'aumento di potenza ad ampio spettro, riportiamo un incremento del PAC tra oscillazioni theta e beta e tra theta e SG in questa linea a 6 mesi. Inoltre, i topi B6.152H mostrano una forte pendenza del power spectrum rispetto ai topi wt a 3 e 6 mesi di età . Sia l'overcoupling che l'incremento della pendenza spettrale sono riconducibili ad una condizione di iper-sincronicità neuronale, anche se con differenze importanti (Voytek and Knight 2015). E' da notare che la differenza tra topi B6.152H e wt in termini di pendenza spettrale è pi๠marcata a 3 mesi di età e diminuisce con l'invecchiamento. Pertanto, anche se ulteriori indagini saranno necessarie per convalidare questa osservazione, l'ipersincronicità del network ippocampale sembra essere un promettente marcatore precoce della malattia, almeno nel contesto di alti livelli di Aß.

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Tipo di EPrint:Tesi di dottorato
Relatore:Fasolato, Cristina
Dottorato (corsi e scuole):Ciclo 28 > Scuole 28 > BIOSCIENZE E BIOTECNOLOGIE > NEUROBIOLOGIA
Data di deposito della tesi:01 Febbraio 2016
Anno di Pubblicazione:01 Febbraio 2016
Parole chiave (italiano / inglese):Alzheimer, presenilin, urethane, oscillations, spectrum, hyperactivity
Settori scientifico-disciplinari MIUR:Area 05 - Scienze biologiche > BIO/09 Fisiologia
Struttura di riferimento:Dipartimenti > Dipartimento di Scienze Biomediche
Codice ID:9543
Depositato il:10 Ott 2016 10:25
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I riferimenti della bibliografia possono essere cercati con Cerca la citazione di AIRE, copiando il titolo dell'articolo (o del libro) e la rivista (se presente) nei campi appositi di "Cerca la Citazione di AIRE".
Le url contenute in alcuni riferimenti sono raggiungibili cliccando sul link alla fine della citazione (Vai!) e tramite Google (Ricerca con Google). Il risultato dipende dalla formattazione della citazione.

Adeli H and Ghosh-Dastidar S. 2010. Automated EEG-based diagnosis of neurological disorders: Inventing the future of neurology. CRC Press. Cerca con Google

Agostini M and Fasolato C. 2016. What players are taking part on Ca2+ homeostasis dysregulation in AD? In: The cellular players in alzheimer's disease: One for all and all for one. Solé M and Milano-Molina AJ, editors. OMICS Group International. Cerca con Google

Alzheimer A. 1911. Uber eigenartige krankheitsfU¤lle des spU¤teren alters. Zeitschrift Fur Die Gesamte Neurologie Und Psychiatrie 4(1):356-85. Cerca con Google

Alzheimer A. 1907. Uber eine eigenartige erkrankung der hirnrinde. Allgemeine Zeitschrife Psychiatrie 64:146-8. Cerca con Google

Alzheimer's Association,. 2015. 2015 alzheimer's disease facts and figures. Alzheimer's & Dementia: The Journal of the Alzheimer's Association 11(3):332-84. Cerca con Google

Amatniek JC, Hauser WA, DelCastillo-Castaneda C, Jacobs DM, Marder K, Bell K, Albert M, Brandt J, Stern Y. 2006. Incidence and predictors of seizures in patients with alzheimer's disease. Epilepsia 47(5):867-72. Cerca con Google

American Psychiatric Association. 2013. Diagnostic and statistical manual of mental disorders (DSM-5'®). American Psychiatric Pub. Cerca con Google

Andersen P, Morris R, Amaral D, Bliss T, O'Keefe J. 2006. The hippocampus book. Oxford University Press, USA. Cerca con Google

Andreasen N and Zetterberg H. 2008. Amyloid-related biomarkers for alzheimer's disease. Curr Med Chem 15(8):766-71. Cerca con Google

Aru J, Aru J, Priesemann V, Wibral M, Lana L, Pipa G, Singer W, Vicente R. 2015. Untangling cross-frequency coupling in neuroscience. Curr Opin Neurobiol 31:51-61. Cerca con Google

Axmacher N, Henseler MM, Jensen O, Weinreich I, Elger CE, Fell J. 2010. Cross-frequency coupling supports multi-item working memory in the human hippocampus. Proc Natl Acad Sci U S A 107(7):3228-33. Cerca con Google

Bakker A, Krauss GL, Albert MS, Speck CL, Jones LR, Stark CE, Yassa MA, Bassett SS, Shelton AL, Gallagher M. 2012. Reduction of hippocampal hyperactivity improves cognition in amnestic mild cognitive impairment. Neuron 74(3):467-74. Cerca con Google

Bassett SS, Yousem DM, Cristinzio C, Kusevic I, Yassa MA, Caffo BS, Zeger SL. 2006. Familial risk for alzheimer's disease alters fMRI activation patterns. Brain 129(Pt 5):1229-39. Cerca con Google

Belluscio MA, Mizuseki K, Schmidt R, Kempter R, Buzsaki G. 2012. Cross-frequency phase-phase coupling between theta and gamma oscillations in the hippocampus. J Neurosci 32(2):423-35. Cerca con Google

Bennys K, Rondouin G, Vergnes C, Touchon J. 2001. Diagnostic value of quantitative EEG in alzheimer's disease. Neurophysiologie Clinique/Clinical Neurophysiology 31(3):153-60. Cerca con Google

Bentahir M, Nyabi O, Verhamme J, Tolia A, Horré K, Wiltfang J, Esselmann H, Strooper B. 2006. Presenilin clinical mutations can affect γ-secretase activity by different mechanisms. J Neurochem 96(3):732-42. Cerca con Google

Benzinger TL, Blazey T, Jack CR,Jr, Koeppe RA, Su Y, Xiong C, Raichle ME, Snyder AZ, Ances BM, Bateman RJ, et al. 2013. Regional variability of imaging biomarkers in autosomal dominant alzheimer's disease. Proc Natl Acad Sci U S A 110(47):E4502-9. Cerca con Google

Berger H. 1929. Uer das elektrenkephalogramm des menschen. Eur Arch Psychiatry Clin Neurosci 87(1):527-70. Cerca con Google

Bertram L and Tanzi R. 2011. Genetics of alzheimer's disease. Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders :51-91. Cerca con Google

Besthorn C, Zerfass R, Geiger-Kabisch C, Sattel H, Daniel S, Schreiter-Gasser U, Forstl H. 1997. Discrimination of alzheimer's disease and normal aging by EEG data. Electroencephalogr Clin Neurophysiol 103(2):241-8. Cerca con Google

Bezprozvanny I. 2009. Calcium signaling and neurodegenerative diseases. Trends Mol Med 15(3):89-100. Cerca con Google

Blennow K. 2004. Cerebrospinal fluid protein biomarkers for alzheimer's disease. NeuroRx 1(2):213-25. Cerca con Google

Borchelt DR, Davis J, Fischer M, Lee MK, Slunt HH, Ratovitsky T, Regard J, Copeland NG, Jenkins NA, Sisodia SS. 1996. A vector for expressing foreign genes in the brains and hearts of transgenic mice. Genet Anal : Biomol Eng 13(6):159-63. Cerca con Google

Born HA, Kim JY, Savjani RR, Das P, Dabaghian YA, Guo Q, Yoo JW, Schuler DR, Cirrito JR, Zheng H, et al. 2014. Genetic suppression of transgenic APP rescues hypersynchronous network activity in a mouse model of alzeimer's disease. J Neurosci 34(11):3826-40. Cerca con Google

Bossers K, Wirz KT, Meerhoff GF, Essing AH, van Dongen JW, Houba P, Kruse CG, Verhaagen J, Swaab DF. 2010. Concerted changes in transcripts in the prefrontal cortex precede neuropathology in alzheimer's disease. Brain 133(Pt 12):3699-723. Cerca con Google

Braak H and Braak E. 1998. Evolution of neuronal changes in the course of alzheimer's disease. Springer. Cerca con Google

Braak H and Braak E. 1997. Frequency of stages of alzheimer-related lesions in different age categories. Neurobiol Aging 18(4):351-7. Cerca con Google

Bragin A, Jando G, Nadasdy Z, Hetke J, Wise K, Buzsaki G. 1995. Gamma (40-100 hz) oscillation in the hippocampus of the behaving rat. J Neurosci 15(1 Pt 1):47-60. Cerca con Google

Brunello L, Zampese E, Florean C, Pozzan T, Pizzo P, Fasolato C. 2009. Presenilin-2 dampens intracellular Ca2 stores by increasing Ca2 leakage and reducing Ca2 uptake. J Cell Mol Med 13(9b):3358-69. Cerca con Google

Buckner RL, Snyder AZ, Shannon BJ, LaRossa G, Sachs R, Fotenos AF, Sheline YI, Klunk WE, Mathis CA, Morris JC, et al. 2005. Molecular, structural, and functional characterization of alzheimer's disease: Evidence for a relationship between default activity, amyloid, and memory. J Neurosci 25(34):7709-17. Cerca con Google

Busche MA, Grienberger C, Keskin AD, Song B, Neumann U, Staufenbiel M, Forstl H, Konnerth A. 2015. Decreased amyloid-[beta] and increased neuronal hyperactivity by immunotherapy in alzheimer's models. Nat Neurosci . Cerca con Google

Busche MA, Chen X, Henning HA, Reichwald J, Staufenbiel M, Sakmann B, Konnerth A. 2012. Critical role of soluble amyloid-beta for early hippocampal hyperactivity in a mouse model of alzheimer's disease. Proc Natl Acad Sci U S A 109(22):8740-5. Cerca con Google

Busche MA, Eichhoff G, Adelsberger H, Abramowski D, Wiederhold KH, Haass C, Staufenbiel M, Konnerth A, Garaschuk O. 2008. Clusters of hyperactive neurons near amyloid plaques in a mouse model of alzheimer's disease. Science 321(5896):1686-9. Cerca con Google

BuzsU¡ki G, Buhl D, Harris K, Csicsvari J, Czeh B, Morozov A. 2003. Hippocampal network patterns of activity in the mouse. Neuroscience 116(1):201-11. Cerca con Google

BuzsU¡ki G, Czopf J, Kondakor I, Kellenyi L. 1986. Laminar distribution of hippocampal rhythmic slow activity (RSA) in the behaving rat: Current-source density analysis, effects of urethane and atropine. Brain Res 365(1):125-37. Cerca con Google

Buzsaki G. 2006. Rhythms of the brain. Oxford University Press. Cerca con Google

BuzsU¡ki G. 2002. Theta oscillations in the hippocampus. Neuron 33(3):325-40. Cerca con Google

BuzsU¡ki G and Wang X. 2012. Mechanisms of gamma oscillations. Annu Rev Neurosci 35:203-25. Cerca con Google

BuzsU¡ki G and Draguhn A. 2004. Neuronal oscillations in cortical networks. Science 304(5679):1926-9. Cerca con Google

BuzsU¡ki G, Logothetis N, Singer W. 2013. Scaling brain size, keeping timing: Evolutionary preservation of brain rhythms. Neuron 80(3):751-64. Cerca con Google

BuzsU¡ki G, Anastassiou CA, Koch C. 2012. The origin of extracellular fields and currents-EEG, ECoG, LFP and spikes. Nature Reviews Neuroscience 13(6):407-20. Cerca con Google

Camandola S and Mattson MP. 2011. Aberrant subcellular neuronal calcium regulation in aging and alzheimer's disease. Biochimica Et Biophysica Acta (BBA)-Molecular Cell Research 1813(5):965-73. Cerca con Google

Canolty RT and Knight RT. 2010. The functional role of cross-frequency coupling. Trends Cogn Sci (Regul Ed ) 14(11):506-15. Cerca con Google

Canolty RT, Edwards E, Dalal SS, Soltani M, Nagarajan SS, Kirsch HE, Berger MS, Barbaro NM, Knight RT. 2006. High gamma power is phase-locked to theta oscillations in human neocortex. Science 313(5793):1626-8. Cerca con Google

Cardin JA, Carlén M, Meletis K, Knoblich U, Zhang F, Deisseroth K, Tsai L, Moore CI. 2009. Driving fast-spiking cells induces gamma rhythm and controls sensory responses. Nature 459(7247):663-7. Cerca con Google

Caroni P. 1997. Overexpression of growth-associated proteins in the neurons of adult transgenic mice. J Neurosci Methods 71(1):3-9. Cerca con Google

Celone KA, Calhoun VD, Dickerson BC, Atri A, Chua EF, Miller SL, DePeau K, Rentz DM, Selkoe DJ, Blacker D, et al. 2006. Alterations in memory networks in mild cognitive impairment and alzheimer's disease: An independent component analysis. J Neurosci 26(40):10222-31. Cerca con Google

Chen X, Li M, Wang S, Zhu H, Xiong Y, Liu X. 2014. Pittsburgh compound B retention and progression of cognitive status- meta-analysis. European Journal of Neurology 21(8):1060-7. Cerca con Google

Chin J., Ling HP, Comery T., Pangalos M., Reinhart P. and Wood A. 2008. Chronic imbalance in neuronal activity and compensatory plasticity are associated with cognitive impairment in Tg2576 and PS1/APP mouse models of alzheimer's disease. International conference on alzheimer's disease. Cerca con Google

Clement EA, Richard A, Thwaites M, Ailon J, Peters S, Dickson CT. 2008. Cyclic and sleep-like spontaneous alternations of brain state under urethane anaesthesia. PLoS One 3(4):e2004. Cerca con Google

Colgin LL and Moser EI. 2010. Gamma oscillations in the hippocampus. Physiology (Bethesda) 25(5):319-29. Cerca con Google

Craig MT and McBain CJ. 2015. Navigating the circuitry of the brain's GPS system: Future challenges for neurophysiologists. Hippocampus . Cerca con Google

Crystal HA, Dickson DW, Sliwinski MJ, Lipton RB, Grober E, Marks-Nelson H, Antis P. 1993. Pathological markers associated with normal aging and dementia in the elderly. Ann Neurol 34(4):566-73. Cerca con Google

Csicsvari J, Jamieson B, Wise KD, BuzsU¡ki G. 2003. Mechanisms of gamma oscillations in the hippocampus of the behaving rat. Neuron 37(2):311-22. Cerca con Google

Cui Y, Liu B, Luo S, Zhen X, Fan M, Liu T, Zhu W, Park M, Jiang T, Jin JS. 2011. Identification of conversion from mild cognitive impairment to alzheimer's disease using multivariate predictors. PloS One 6(7):e21896. Cerca con Google

Dauwels J, Vialatte F, Cichocki A. 2010. Diagnosis of alzheimer's disease from EEG signals: Where are we standing? Current Alzheimer Research 7(6):487-505. Cerca con Google

Davis D, Schmitt F, Wekstein D, Markesbery W. 1999. Alzheimer neuropathologic alterations in aged cognitively normal subjects. Journal of Neuropathology & Experimental Neurology 58(4):376-88. Cerca con Google

Del Prete D, Checler F, Chami M. 2014. Ryanodine receptors: Physiological function and deregulation in alzheimer disease. Mol.Neurodegener 9:21. Cerca con Google

Del Vecchio RA, Gold LH, Novick SJ, Wong G, Hyde LA. 2004. Increased seizure threshold and severity in young transgenic CRND8 mice. Neurosci Lett 367(2):164-7. Cerca con Google

Depuy SD, Kanbar R, Coates MB, Stornetta RL, Guyenet PG. 2011. Control of breathing by raphe obscurus serotonergic neurons in mice. J Neurosci 31(6):1981-90. Cerca con Google

Di Fede G, Catania M, Morbin M, Rossi G, Suardi S, Mazzoleni G, Merlin M, Giovagnoli AR, Prioni S, Erbetta A, et al. 2009. A recessive mutation in the APP gene with dominant-negative effect on amyloidogenesis. Science 323(5920):1473-7. Cerca con Google

Dickerson BC, Salat DH, Greve DN, Chua EF, Rand-Giovannetti E, Rentz DM, Bertram L, Mullin K, Tanzi RE, Blacker D, et al. 2005. Increased hippocampal activation in mild cognitive impairment compared to normal aging and AD. Neurology 65(3):404-11. Cerca con Google

Dubelaar EJ, Mufson EJ, ter Meulen WG, Van Heerikhuize JJ, Verwer RW, Swaab DF. 2006. Increased metabolic activity in nucleus basalis of meynert neurons in elderly individuals with mild cognitive impairment as indicated by the size of the golgi apparatus. J Neuropathol Exp Neurol 65(3):257-66. Cerca con Google

Duyckaerts C, Potier M, Delatour B. 2008. Alzheimer disease models and human neuropathology: Similarities and differences. Acta Neuropathol 115(1):5-38. Cerca con Google

Ewers M, Sperling RA, Klunk WE, Weiner MW, Hampel H. 2011. Neuroimaging markers for the prediction and early diagnosis of alzheimer's disease dementia. Trends Neurosci 34(8):430-42. Cerca con Google

Fedele E, Rivera D, Marengo B, Pronzato MA, Ricciarelli R. 2015. Amyloid ß: Walking on the dark side of the moon. Mech Ageing Dev 152:1-4. Cerca con Google

Fell J, Ludowig E, Staresina BP, Wagner T, Kranz T, Elger CE, Axmacher N. 2011. Medial temporal theta/alpha power enhancement precedes successful memory encoding: Evidence based on intracranial EEG. J Neurosci 31(14):5392-7. Cerca con Google

Fischer P. 1907. Miliare nekrosen mit drusigen wucherungen der neurofibrillen, eine regelmU¤ssige verU¤nderung der hirnrinde bei seniler demenz. Eur Neurol 22(4):361-72. Cerca con Google

Forlenza OV, Diniz BS, Gattaz WF. 2010. Diagnosis and biomarkers of predementia in alzheimer's disease. BMC Med 8:89,7015-8-89. Cerca con Google

Franca AS, Nascimento GC, Lopes-dos-Santos V, Muratori L, Ribeiro S, Lobao-Soares B, Tort AB. 2014. Beta2 oscillations (23-30 hz) in the mouse hippocampus during novel object recognition. Eur J Neurosci 40(11):3693-703. Cerca con Google

Freeman WJ. 2007. Definitions of state variables and state space for brain-computer interface. Cognitive Neurodynamics 1(1):3-14. Cerca con Google

Freeman WJ and Zhai J. 2009. Simulated power spectral density (PSD) of background electrocorticogram (ECoG). Cognitive Neurodynamics 3(1):97-103. Cerca con Google

Gandy S. 2005. The role of cerebral amyloid beta accumulation in common forms of alzheimer disease. J Clin Invest 115(5):1121-9. Cerca con Google

Giacomello M, Barbiero L, Zatti G, Squitti R, Binetti G, Pozzan T, Fasolato C, Ghidoni R, Pizzo P. 2005. Reduction of ca 2 stores and capacitative ca 2 entry is associated with the familial alzheimer's disease presenilin-2 T122R mutation and anticipates the onset of dementia. Neurobiol Dis 18(3):638-48. Cerca con Google

Giannakopoulos P, Herrmann FR, Bussiere T, Bouras C, Kovari E, Perl DP, Morrison JH, Gold G, Hof PR. 2003. Tangle and neuron numbers, but not amyloid load, predict cognitive status in alzheimer's disease. Neurology 60(9):1495-500. Cerca con Google

Glenner G and Wong C. 1984. Alzheimer's disease: Initial report of the purification andcharacterization of a novel cerebrovascular amyloid protein. biochem. biophys. res. com-mun. 120, 885-890. Glenner885120Biochem.Biophys.Res.Commun. Cerca con Google

Goate A, Chartier-Harlin M, Mullan M, Brown J, Crawford F, Fidani L, Giuffra L, Haynes A, Irving N, James L. 1991. Segregation of a missense mutation in the amyloid precursor protein gene with familial alzheimer's disease. Nature 349(6311):704-6. Cerca con Google

Goedert M, Wischik CM, Crowther RA, Walker JE, Klug A. 1988. Cloning and sequencing of the cDNA encoding a core protein of the paired helical filament of alzheimer disease: Identification as the microtubule-associated protein tau. Proc Natl Acad Sci U S A 85(11):4051-5. Cerca con Google

Golde TE, Schneider LS, Koo EH. 2011. Anti-aß therapeutics in alzheimer's disease: The need for a paradigm shift. Neuron 69(2):203-13. Cerca con Google

Gosche KM, Mortimer JA, Smith CD, Markesbery WR, Snowdon DA. 2002. Hippocampal volume as an index of alzheimer neuropathology: Findings from the nun study. Neurology 58(10):1476-82. Cerca con Google

Graeber M, Kosel S, Grasbon-Frodl E, Moller H, Mehraein P. 1998. Histopathology and APOE genotype of the first alzheimer disease patient, auguste D. Neurogenetics 1(3):223-8. Cerca con Google

Grunwald M, Busse F, Hensel A, Kruggel F, Riedel'Heller S, Wolf H, Arendt T, Gertz H. 2001. Correlation between cortical θ activity and hippocampal volumes in health, mild cognitive impairment, and mild dementia. Journal of Clinical Neurophysiology 18(2):178-84. Cerca con Google

Guerreiro R and Hardy J. 2014. Genetics of alzheimer's disease. Neurotherapeutics 11(4):732-7. Cerca con Google

Gyure KA, Durham R, Stewart WF, Smialek JE, Troncoso JC. 2001. Intraeuronal abeta-amyloid precedes development of amyloid plaques in down syndrome. Arch Pathol Lab Med 125(4):489. Cerca con Google

HU¤mU¤lU¤inen A, PihlajamU¤ki M, Tanila H, HU¤nninen T, Niskanen E, Tervo S, Karjalainen PA, Vanninen RL, Soininen H. 2007. Increased fMRI responses during encoding in mild cognitive impairment. Neurobiol Aging 28(12):1889-903. Cerca con Google

Hampel H, Teipel S, Fuchsberger T, Andreasen N, Wiltfang J, Otto M, Shen Y, Dodel R, Du Y, Farlow M. 2004. Value of CSF ß-amyloid1'42 and tau as predictors of alzheimer's disease in patients with mild cognitive impairment. Mol Psychiatry 9(7):705-10. Cerca con Google

Hara K and Harris RA. 2002. The anesthetic mechanism of urethane: The effects on neurotransmitter-gated ion channels. Anesthesia & Analgesia 94(2):313-8. Cerca con Google

Hardy J. 2006. A hundred years of alzheimer's disease research. Neuron 52(1):3-13. Cerca con Google

Hardy JA and Higgins GA. 1992. Alzheimer's disease: The amyloid cascade hypothesis. Science 256(5054):184. Cerca con Google

Hardy J and Selkoe DJ. 2002. The amyloid hypothesis of alzheimer's disease: Progress and problems on the road to therapeutics. Science 297(5580):353-6. Cerca con Google

Harrison JR and Owen MJ. 2016. Alzheimer's disease: The amyloid hypothesis on trial. Br J Psychiatry 208(1):1-3. Cerca con Google

Hass Matthew R., Sato Chihiro, Kopan Raphael and Zhao Guojun. 2009. Presenilin: RIP and beyond. Seminars in cell & developmental biologyElsevier. 201 p. Cerca con Google

Hayrapetyan V, Rybalchenko V, Rybalchenko N, Koulen P. 2008. The N-terminus of presenilin-2 increases single channel activity of brain ryanodine receptors through direct protein' protein interaction. Cell Calcium 44(5):507-18. Cerca con Google

He BJ. 2014. Scale-free brain activity: Past, present, and future. Trends Cogn Sci (Regul Ed ) 18(9):480-7. Cerca con Google

He BJ, Zempel JM, Snyder AZ, Raichle ME. 2010. The temporal structures and functional significance of scale-free brain activity. Neuron 66(3):353-69. Cerca con Google

He BJ, Snyder AZ, Zempel JM, Smyth MD, Raichle ME. 2008. Electrophysiological correlates of the brain's intrinsic large-scale functional architecture. Proc Natl Acad Sci U S A 105(41):16039-44. Cerca con Google

Herrup K. 2015. The case for rejecting the amyloid cascade hypothesis. Nat Neurosci :794-9. Cerca con Google

Holscher C, Anwyl R, Rowan MJ. 1997. Stimulation on the positive phase of hippocampal theta rhythm induces long-term potentiation that can be depotentiated by stimulation on the negative phase in area CA1 in vivo. J Neurosci 17(16):6470-7. Cerca con Google

Honarnejad K and Herms J. 2012. Presenilins: Role in calcium homeostasis. Int J Biochem Cell Biol 44(11):1983-6. Cerca con Google

Huang C, Wahlund L, Dierks T, Julin P, Winblad B, Jelic V. 2000. Discrimination of alzheimer's disease and mild cognitive impairment by equivalent EEG sources: A cross-sectional and longitudinal study. Clinical Neurophysiology 111(11):1961-7. Cerca con Google

Huang Y, Yang S, Hu Z, Liu G, Zhou W, Zhang Y. 2012. A new approach to location of the dentate gyrus and perforant path in rats/mice by landmarks on the skull. Acta Neurobiol Exp 72:468-72. Cerca con Google

International Federation of Societies for Electroencephalography and Clinical Neurophysiology. 1974. Electroencephalography and Clinical Neurophysiology 37:521-3. Cerca con Google

Ittner AA, Gladbach A, Bertz J, Suh LS, Ittner LM. 2014. p38 MAP kinase-mediated NMDA receptor-dependent suppression of hippocampal hypersynchronicity in a mouse model of alzheimer's disease. Acta Neuropathologica Communications 2(1):1-17. Cerca con Google

Jack CR,Jr, Albert MS, Knopman DS, McKhann GM, Sperling RA, Carrillo MC, Thies B, Phelps CH. 2011. Introduction to the recommendations from the national institute on aging-alzheimer's association workgroups on diagnostic guidelines for alzheimer's disease. Alzheimers Dement 7(3):257-62. Cerca con Google

Jagust W. 2016. Is amyloid-beta harmful to the brain? insights from human imaging studies. Brain 139(Pt 1):23-30. Cerca con Google

James W. 1890. The principles of psychology. . Cerca con Google

Jayadev S, Leverenz JB, Steinbart E, Stahl J, Klunk W, Yu CE, Bird TD. 2010. Alzheimer's disease phenotypes and genotypes associated with mutations in presenilin 2. Brain 133(Pt 4):1143-54. Cerca con Google

Jelic V, Johansson S, Almkvist O, Shigeta M, Julin P, Nordberg A, Winblad B, Wahlund L. 2000. Quantitative electroencephalography in mild cognitive impairment: Longitudinal changes and possible prediction of alzheimer'€™s disease. Neurobiol Aging 21(4):533-40. Cerca con Google

Johnson S, Schmitz T, Moritz C, Meyerand M, Rowley H, Alexander A, Hansen K, Gleason C, Carlsson C, Ries M. 2006. Activation of brain regions vulnerable to alzheimer's disease: The effect of mild cognitive impairment. Neurobiol Aging 27(11):1604-12. Cerca con Google

Jonsson T, Atwal JK, Steinberg S, Snaedal J, Jonsson PV, Bjornsson S, Stefansson H, Sulem P, Gudbjartsson D, Maloney J. 2012. A mutation in APP protects against alzheimer/'s disease and age-related cognitive decline. Nature 488(7409):96-9. Cerca con Google

Kahana MJ, Seelig D, Madsen JR. 2001. Theta returns. Curr Opin Neurobiol 11(6):739-44. Cerca con Google

Kang J, Lemaire H, Unterbeck A, Salbaum JM, Masters CL, Grzeschik K, Multhaup G, Beyreuther K, Muller-Hill B. 1987. The precursor of alzheimer's disease amyloid A4 protein resembles a cell-surface receptor. . Cerca con Google

Katzman R. 1976. The prevalence and malignancy of alzheimer disease: A major killer. Arch Neurol 33(4):217-8. Cerca con Google

Kay LM and Lazzara P. 2010. How global are olfactory bulb oscillations? J Neurophysiol 104(3):1768-73. Cerca con Google

Khachaturian ZS. 1987. Hypothesis on the regulation of cytosol calcium concentration and the aging brain. Neurobiol Aging 8(4):345-6. Cerca con Google

Khan UA, Liu L, Provenzano FA, Berman DE, Profaci CP, Sloan R, Mayeux R, Duff KE, Small SA. 2014. Molecular drivers and cortical spread of lateral entorhinal cortex dysfunction in preclinical alzheimer's disease. Nat Neurosci 17(2):304-11. Cerca con Google

Kipanyula MJ, Contreras L, Zampese E, Lazzari C, Wong AK, Pizzo P, Fasolato C, Pozzan T. 2012. Ca2 dysregulation in neurons from transgenic mice expressing mutant presenilin 2. Aging Cell 11(5):885-93. Cerca con Google

Kirwan CB and Stark CE. 2004. Medial temporal lobe activation during encoding and retrieval of novel face-name pairs. Hippocampus 14(7):919-30. Cerca con Google

Kiss T, Feng J, Hoffmann W, Shaffer C, HajU³s M. 2013. Rhythmic theta and delta activity of cortical and hippocampal neuronal networks in genetically or pharmacologically induced N-methyl-D-aspartate receptor hypofunction under urethane anesthesia. Neuroscience 237:255-67. Cerca con Google

Knopman D, Parisi J, Salviati A, Floriach-Robert M, Boeve B, Ivnik R, Smith G, Dickson D, Johnson K, Petersen L. 2003. Neuropathology of cognitively normal elderly. Journal of Neuropathology & Experimental Neurology 62(11):1087-95. Cerca con Google

Kramis R, Vanderwolf C, Bland BH. 1975. Two types of hippocampal rhythmical slow activity in both the rabbit and the rat: Relations to behavior and effects of atropine, diethyl ether, urethane, and pentobarbital. Exp Neurol 49(1):58-85. Cerca con Google

Kuchibhotla KV, Goldman ST, Lattarulo CR, Wu H, Hyman BT, Bacskai BJ. 2008. Aß plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks. Neuron 59(2):214-25. Cerca con Google

Lai MT, Chen E, Crouthamel MC, DiMuzio-Mower J, Xu M, Huang Q, Price E, Register RB, Shi XP, Donoviel DB, et al. 2003. Presenilin-1 and presenilin-2 exhibit distinct yet overlapping gamma-secretase activities. J Biol Chem 278(25):22475-81. Cerca con Google

Lakatos P, Shah AS, Knuth KH, Ulbert I, Karmos G, Schroeder CE. 2005. An oscillatory hierarchy controlling neuronal excitability and stimulus processing in the auditory cortex. J Neurophysiol 94(3):1904-11. Cerca con Google

Lanz TA, Himes CS, Pallante G, Adams L, Yamazaki S, Amore B, Merchant KM. 2003. The gamma-secretase inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester reduces A beta levels in vivo in plasma and cerebrospinal fluid in young (plaque-free) and aged (plaque-bearing) Tg2576 mice. J Pharmacol Exp Ther 305(3):864-71. Cerca con Google

Lau P, Bossers K, Janky R, Salta E, Frigerio CS, Barbash S, Rothman R, Sierksma AS, Thathiah A, Greenberg D, et al. 2013. Alteration of the microRNA network during the progression of alzheimer's disease. EMBO Mol Med 5(10):1613-34. Cerca con Google

Lawson VH and Bland BH. 1993. The role of the septohippocampal pathway in the regulation of hippocampal field activity and behavior: Analysis by the intraseptal microinfusion of carbachol, atropine, and procaine. Exp Neurol 120(1):132-44. Cerca con Google

Lee H, Simpson GV, Logothetis NK, Rainer G. 2005. Phase locking of single neuron activity to theta oscillations during working memory in monkey extrastriate visual cortex. Neuron 45(1):147-56. Cerca con Google

Lega BC, Jacobs J, Kahana M. 2012. Human hippocampal theta oscillations and the formation of episodic memories. Hippocampus 22(4):748-61. Cerca con Google

Lega B, Burke J, Jacobs J, Kahana MJ. 2016. Slow-theta-to-gamma phase-amplitude coupling in human hippocampus supports the formation of new episodic memories. Cereb Cortex 26(1):268-78. Cerca con Google

Lesné S, Kotilinek L, Ashe KH. 2008. Plaque-bearing mice with reduced levels of oligomeric amyloid-ß assemblies have intact memory function. Neuroscience 151(3):745-9. Cerca con Google

Lesné S, Koh MT, Kotilinek L, Kayed R, Glabe CG, Yang A, Gallagher M, Ashe KH. 2006. A specific amyloid-ß protein assembly in the brain impairs memory. Nature 440(7082):352-7. Cerca con Google

Leuchter AF, Spar JE, Walter DO, Weiner H. 1987. Electroencephalographic spectra and coherence in the diagnosis of alzheimer's-type and multi-infarct dementia: A pilot study. Arch Gen Psychiatry 44(11):993-8. Cerca con Google

Lima FR, Arantes CP, Muras AG, Nomizo R, Brentani RR, Martins VR. 2007. Cellular prion protein expression in astrocytes modulates neuronal survival and differentiation. J Neurochem 103(6):2164-76. Cerca con Google

Linkenkaer-Hansen K, Nikouline VV, Palva JM, Ilmoniemi RJ. 2001. Long-range temporal correlations and scaling behavior in human brain oscillations. J Neurosci 21(4):1370-7. Cerca con Google

Lisman JE and Jensen O. 2013. The theta-gamma neural code. Neuron 77(6):1002-16. Cerca con Google

Lista S, Garaci FG, Ewers M, Teipel S, Zetterberg H, Blennow K, Hampel H. 2014. CSF Aß1-42 combined with neuroimaging biomarkers in the early detection, diagnosis and prediction of alzheimer's disease. Alzheimer's & Dementia 10(3):381-92. Cerca con Google

Locatelli T, Cursi M, Liberati D, Franceschi M, Comi G. 1998. EEG coherence in alzheimer's disease. Electroencephalogr Clin Neurophysiol 106(3):229-37. Cerca con Google

Logothetis NK, Kayser C, Oeltermann A. 2007. In vivo measurement of cortical impedance spectrum in monkeys: Implications for signal propagation. Neuron 55(5):809-23. Cerca con Google

Lowry CA and Kay LM. 2007. Chemical factors determine olfactory system beta oscillations in waking rats. J Neurophysiol 98(1):394-404. Cerca con Google

Lozsadi DA and Larner AJ. 2006. Prevalence and causes of seizures at the time of diagnosis of probable alzheimer's disease. Dement Geriatr Cogn Disord 22(2):121-4. Cerca con Google

Machulda MM, Ward HA, Borowski B, Gunter JL, Cha RH, O'Brien PC, Petersen RC, Boeve BF, Knopman D, Tang-Wai DF, et al. 2003. Comparison of memory fMRI response among normal, MCI, and alzheimer's patients. Neurology 61(4):500-6. Cerca con Google

Manly JJ, Tang M, Schupf N, Stern Y, Vonsattel JG, Mayeux R. 2008. Frequency and course of mild cognitive impairment in a multiethnic community. Ann Neurol 63(4):494-506. Cerca con Google

Manning JR, Jacobs J, Fried I, Kahana MJ. 2009. Broadband shifts in local field potential power spectra are correlated with single-neuron spiking in humans. J Neurosci 29(43):13613-20. Cerca con Google

Markowska AL, Olton DS, Givens B. 1995. Cholinergic manipulations in the medial septal area: Age-related effects on working memory and hippocampal electrophysiology. J Neurosci 15(3 Pt 1):2063-73. Cerca con Google

Maskri L, Zhu X, Fritzen S, Kuhn K, Ullmer C, Engels P, Andriske M, Stichel CC, Lubbert H. 2004. Influence of different promoters on the expression pattern of mutated human alpha-synuclein in transgenic mice. Neurodegener Dis 1(6):255-65. Cerca con Google

Masliah E, Terry RD, Mallory M, Alford M, Hansen LA. 1990. Diffuse plaques do not accentuate synapse loss in alzheimer's disease. Am J Pathol 137(6):1293-7. Cerca con Google

Masters CL, Simms G, Weinman NA, Multhaup G, McDonald BL, Beyreuther K. 1985. Amyloid plaque core protein in alzheimer disease and down syndrome. Proc Natl Acad Sci U S A 82(12):4245-9. Cerca con Google

Mattsson N, Zetterberg H, Hansson O, Andreasen N, Parnetti L, Jonsson M, Herukka S, van der Flier, Wiesje M, Blankenstein MA, Ewers M. 2009. CSF biomarkers and incipient alzheimer disease in patients with mild cognitive impairment. Jama 302(4):385-93. Cerca con Google

Mattsson N and Zetterberg H. 2009. Future screening for incipient alzheimer's disease--the influence of prevalence on test performance. Eur Neurol 62(4):200-3. Cerca con Google

Maurer K, Volk S, Gerbaldo H. 1997. Auguste D and alzheimer's disease. The Lancet 349(9064):1546-9. Cerca con Google

McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. 1984. Clinical diagnosis of alzheimer's disease: Report of the NINCDS-ADRDA work group under the auspices of department of health and human services task force on alzheimer's disease. Neurology 34(7):939-44. Cerca con Google

Mendes MHF. 2002. Transient epileptic amnesia: An under-diagnosed phenomenon? three more cases. Seizure 11(4):238-42. Cerca con Google

Miller SL, Fenstermacher E, Bates J, Blacker D, Sperling RA, Dickerson BC. 2008. Hippocampal activation in adults with mild cognitive impairment predicts subsequent cognitive decline. J Neurol Neurosurg Psychiatry 79(6):630-5. Cerca con Google

Minkeviciene R, Rheims S, Dobszay MB, Zilberter M, Hartikainen J, Fulop L, Penke B, Zilberter Y, Harkany T, Pitkanen A, et al. 2009. Amyloid beta-induced neuronal hyperexcitability triggers progressive epilepsy. J Neurosci 29(11):3453-62. Cerca con Google

Mitchell AJ, Monge-Argiles JA, Sanchez-Paya J. 2010. Do CSF biomarkers help clinicians predict the progression of mild cognitive impairment to dementia? Pract Neurol 10(4):202-7. Cerca con Google

Moretti D, Miniussi C, Frisoni G, Zanetti O, Binetti G, Geroldi C, Galluzzi S, Rossini P. 2007. Vascular damage and EEG markers in subjects with mild cognitive impairment. Clinical Neurophysiology 118(8):1866-76. Cerca con Google

Moser M, Colello RJ, Pott U, Oesch B. 1995. Developmental expression of the prion protein gene in glial cells. Neuron 14(3):509-17. Cerca con Google

Mukamel R, Gelbard H, Arieli A, Hasson U, Fried I, Malach R. 2005. Coupling between neuronal firing, field potentials, and FMRI in human auditory cortex. Science 309(5736):951-4. Cerca con Google

Muller R, Struck H, Ho M, Brockhaus-Dumke A, Klosterkotter J, Broich K, Hescheler J, Schneider T, WeiergrU¤ber M. 2012. Atropine-sensitive hippocampal theta oscillations are mediated by ca v 2.3 R-type ca 2 channels. Neuroscience 205:125-39. Cerca con Google

Muller U, Winter P, Graeber MB. 2013. A presenilin 1 mutation in the first case of alzheimer's disease. Lancet Neurol 12(2):129-30. Cerca con Google

Namgung U, Valcourt E, Routtenberg A. 1995. Long-term potentiation in vivo in the intact mouse hippocampus. Brain Res 689(1):85-92. Cerca con Google

Nielson DM, Smith TA, Sreekumar V, Dennis S, Sederberg PB. 2015. Human hippocampus represents space and time during retrieval of real-world memories. Proc Natl Acad Sci U S A 112(35):11078-83. Cerca con Google

Nir Y, Fisch L, Mukamel R, Gelbard-Sagiv H, Arieli A, Fried I, Malach R. 2007. Coupling between neuronal firing rate, gamma LFP, and BOLD fMRI is related to interneuronal correlations. Current Biology 17(15):1275-85. Cerca con Google

Nunez P. 1981. Electric fields of the brain. 1981. . Cerca con Google

Oh H, Steffener J, Razlighi QR, Habeck C, Liu D, Gazes Y, Janicki S, Stern Y. 2015. Aß-related hyperactivation in frontoparietal control regions in cognitively normal elderly. Neurobiol Aging 36(12):3247-54. Cerca con Google

Ozmen L, Albientz A, Czech C, Jacobsen H. 2009. Expression of transgenic APP mRNA is the key determinant for beta-amyloid deposition in PS2APP transgenic mice. Neurodegener Dis 6(1-2):29-36. Cerca con Google

Pagliardini S, Gosgnach S, Dickson CT. 2013. Spontaneous sleep-like brain state alternations and breathing characteristics in urethane anesthetized mice. PloS One 8(7):e70411. Cerca con Google

Palop JJ and Mucke L. 2009. Epilepsy and cognitive impairments in alzheimer disease. Arch Neurol 66(4):435-40. Cerca con Google

Palop JJ, Chin J, Mucke L. 2006. A network dysfunction perspective on neurodegenerative diseases. Nature 443(7113):768-73. Cerca con Google

Palop JJ, Chin J, Roberson ED, Wang J, Thwin MT, Bien-Ly N, Yoo J, Ho KO, Yu G, Kreitzer A. 2007. Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of alzheimer's disease. Neuron 55(5):697-711. Cerca con Google

Penny W, Duzel E, Miller K, Ojemann J. 2008. Testing for nested oscillation. J Neurosci Methods 174(1):50-61. Cerca con Google

Penttonen M and BuzsU¡ki G. 2003. Natural logarithmic relationship between brain oscillators. Thalamus & Related Systems 2(02):145-52. Cerca con Google

PernU­a-Andrade AJ and Jonas P. 2014. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron 81(1):140-52. Cerca con Google

Perusini G. 1909. Uber klinisch und histologisch eigenartige psychische erkrankungen des spU¤teren lebensalters. Histologische Und Histopathologische Arbeiten.Jena: Verlag G Fischer :297-351. Cerca con Google

Petersen RC, Doody R, Kurz A, Mohs RC, Morris JC, Rabins PV, Ritchie K, Rossor M, Thal L, Winblad B. 2001. Current concepts in mild cognitive impairment. Arch Neurol 58(12):1985-92. Cerca con Google

Pihlajamaki M, Jauhiainen AM, Soininen H. 2009. Structural and functional MRI in mild cognitive impairment. Current Alzheimer Research 6(2):179-85. Cerca con Google

Podvalny E, Noy N, Harel M, Bickel S, Chechik G, Schroeder CE, Mehta AD, Tsodyks M, Malach R. 2015. A unifying principle underlying the extracellular field potential spectral responses in the human cortex. J Neurophysiol :jn. 00943.2014. Cerca con Google

Poil S, De Haan W, van der Flier, Wiesje M, Mansvelder HD, Scheltens P, Linkenkaer-Hansen K. 2013. Integrative EEG biomarkers predict progression to alzheimer's disease at the MCI stage. Frontiers in Aging Neuroscience 5. Cerca con Google

Poirier R, Veltman I, Pflimlin MC, Knoflach F, Metzger F. 2010. Enhanced dentate gyrus synaptic plasticity but reduced neurogenesis in a mouse model of amyloidosis. Neurobiol Dis 40(2):386-93. Cerca con Google

Price JL and Morris JC. 1999. Tangles and plaques in nondemented aging and" preclinical" alzheimer's disease. Ann Neurol 45(3):358-68. Cerca con Google

Price JL, Davis P, Morris J, White D. 1991. The distribution of tangles, plaques and related immunohistochemical markers in healthy aging and alzheimer's disease. Neurobiol Aging 12(4):295-312. Cerca con Google

Pucci E, Belardinelli N, Cacchio G, Signorino M, Angeleri F. 1999. EEG power spectrum differences in early and late onset forms of alzheimer's disease. Clinical Neurophysiology 110(4):621-31. Cerca con Google

Purves D. 2004. Neuroscience. Sinauer Associates Inc. Cerca con Google

Putcha D, Brickhouse M, O'Keefe K, Sullivan C, Rentz D, Marshall G, Dickerson B, Sperling R. 2011. Hippocampal hyperactivation associated with cortical thinning in alzheimer's disease signature regions in non-demented elderly adults. J Neurosci 31(48):17680-8. Cerca con Google

Puzzo D, Gulisano W, Arancio O, Palmeri A. 2015. The keystone of alzheimer pathogenesis might be sought in aß physiology. Neuroscience 307:26-36. Cerca con Google

Quiroz YT, Budson AE, Celone K, Ruiz A, Newmark R, CastrillU³n G, Lopera F, Stern CE. 2010. Hippocampal hyperactivation in presymptomatic familial alzheimer's disease. Ann Neurol 68(6):865-75. Cerca con Google

Rabinowicz AL, Starkstein SE, Leiguarda RC, Coleman AE. 2000. Transient epileptic amnesia in dementia: A treatable unrecognized cause of episodic amnestic wandering. Alzheimer Disease & Associated Disorders 14(4):231-3. Cerca con Google

Rasch MJ, Gretton A, Murayama Y, Maass W, Logothetis NK. 2008. Inferring spike trains from local field potentials. J Neurophysiol 99(3):1461-76. Cerca con Google

Ray WJ and Cole HW. 1985. EEG alpha activity reflects attentional demands, and beta activity reflects emotional and cognitive processes. Science 228(4700):750-2. Cerca con Google

Richards JG, Higgins GA, Ouagazzal AM, Ozmen L, Kew JN, Bohrmann B, Malherbe P, Brockhaus M, Loetscher H, Czech C, et al. 2003. PS2APP transgenic mice, coexpressing hPS2mut and hAPPswe, show age-related cognitive deficits associated with discrete brain amyloid deposition and inflammation. J Neurosci 23(26):8989-9003. Cerca con Google

Riley KP, Snowdon DA, Markesbery WR. 2002. Alzheimer's neurofibrillary pathology and the spectrum of cognitive function: Findings from the nun study. Ann Neurol 51(5):567-77. Cerca con Google

Roberson ED, Scearce-Levie K, Palop JJ, Yan F, Cheng IH, Wu T, Gerstein H, Yu GQ, Mucke L. 2007. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an alzheimer's disease mouse model. Science 316(5825):750-4. Cerca con Google

RodrU­guez-Arellano J, Parpura V, Zorec R, Verkhratsky A. 2015. Astrocytes in physiological aging and alzheimer's disease. Neuroscience . Cerca con Google

Rodriguez-Vieitez E, et al. 2016. Diverging longitudinal changes in astrocytosis and amyloid PET in autosomal dominant alzheimer's disease. Brain : A Journal of Neurology JID - 0372537 OTO - NOTNLM . Cerca con Google

Rogaev E, Sherrington R, Rogaeva E, Levesque G, Ikeda M, Liang Y, Chi H, Lin C, Holman K, Tsuda T. 1995. Familial alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the alzheimer's disease type 3 gene. Nature 376(6543):775-8. Cerca con Google

Rossini P, Del Percio C, Pasqualetti P, Cassetta E, Binetti G, Dal Forno G, Ferreri F, Frisoni G, Chiovenda P, Miniussi C. 2006. Conversion from mild cognitive impairment to alzheimer's disease is predicted by sources and coherence of brain electroencephalography rhythms. Neuroscience 143(3):793-803. Cerca con Google

Rubio SE, Vega-Flores G, Martinez A, Bosch C, Perez-Mediavilla A, del Rio J, Gruart A, Delgado-Garcia JM, Soriano E, Pascual M. 2012. Accelerated aging of the GABAergic septohippocampal pathway and decreased hippocampal rhythms in a mouse model of alzheimer's disease. Faseb J 26(11):4458-67. Cerca con Google

Rupp C, Beyreuther K, Maurer K, Kins S. 2014. A presenilin 1 mutation in the first case of alzheimer's disease: Revisited. Alzheimer's & Dementia 10(6):869-72. Cerca con Google

Ryan NS, Rossor MN, Fox NC. 2015. Alzheimer's disease in the 100 years since alzheimer's death. Brain :awv316. Cerca con Google

Sanchez PE, Zhu L, Verret L, Vossel KA, Orr AG, Cirrito JR, Devidze N, Ho K, Yu G, Palop JJ. 2012. Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an alzheimer's disease model. Proceedings of the National Academy of Sciences 109(42):E2895-903. Cerca con Google

Saunders AM, Strittmatter WJ, Schmechel D, George-Hyslop PH, Pericak-Vance MA, Joo SH, Rosi BL, Gusella JF, Crapper-MacLachlan DR, Alberts MJ. 1993. Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic alzheimer's disease. Neurology 43(8):1467-72. Cerca con Google

Sceniak MP and MacIver MB. 2006. Cellular actions of urethane on rat visual cortical neurons in vitro. J Neurophysiol 95(6):3865-74. Cerca con Google

Scheffer-Teixeira R, Belchior H, Leao RN, Ribeiro S, Tort AB. 2013. On high-frequency field oscillations (>100 hz) and the spectral leakage of spiking activity. J Neurosci 33(4):1535-9. Cerca con Google

Scheffer-Teixeira R, Belchior H, Caixeta FV, Souza BC, Ribeiro S, Tort AB. 2012. Theta phase modulates multiple layer-specific oscillations in the CA1 region. Cereb Cortex 22(10):2404-14. Cerca con Google

Schmidt R, Kienbacher E, Benke T, Dal-Bianco P, Delazer M, Ladurner G, Jellinger K, Marksteiner J, Ransmayr G, Schmidt H, et al. 2008. Sex differences in alzheimer's disease. Neuropsychiatr 22(1):1-15. Cerca con Google

Schoonenboom NS, Mulder C, Van Kamp GJ, Mehta SP, Scheltens P, Blankenstein MA, Mehta PD. 2005. Amyloid ß 38, 40, and 42 species in cerebrospinal fluid: More of the same? Ann Neurol 58(1):139-42. Cerca con Google

Sederberg PB, Schulze-Bonhage A, Madsen JR, Bromfield EB, Litt B, Brandt A, Kahana MJ. 2007a. Gamma oscillations distinguish true from false memories. Psychol Sci 18(11):927-32. Cerca con Google

Sederberg PB, Schulze-Bonhage A, Madsen JR, Bromfield EB, McCarthy DC, Brandt A, Tully MS, Kahana MJ. 2007b. Hippocampal and neocortical gamma oscillations predict memory formation in humans. Cereb Cortex 17(5):1190-6. Cerca con Google

Selkoe DJ. 1991. The molecular pathology of alzheimer's disease. Neuron 6(4):487-98. Cerca con Google

Selkoe DJ and Wolfe MS. 2007. Presenilin: Running with scissors in the membrane. Cell 131(2):215-21. Cerca con Google

Shankar GM, Li S, Mehta TH, Garcia-Munoz A, Shepardson NE, Smith I, Brett FM, Farrell MA, Rowan MJ, Lemere CA. 2008. Amyloid-ß protein dimers isolated directly from alzheimer's brains impair synaptic plasticity and memory. Nat Med 14(8):837-42. Cerca con Google

Shankar GM, Bloodgood BL, Townsend M, Walsh DM, Selkoe DJ, Sabatini BL. 2007. Natural oligomers of the alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway. J Neurosci 27(11):2866-75. Cerca con Google

Shen J and Kelleher RJ,3rd. 2007. The presenilin hypothesis of alzheimer's disease: Evidence for a loss-of-function pathogenic mechanism. Proc Natl Acad Sci U S A 104(2):403-9. Cerca con Google

Shilling D, Mak DO, Kang DE, Foskett JK. 2012. Lack of evidence for presenilins as endoplasmic reticulum Ca2+ leak channels. J Biol Chem 287(14):10933-44. Cerca con Google

Shin J, Kim D, Bianchi R, Wong RK, Shin HS. 2005. Genetic dissection of theta rhythm heterogeneity in mice. Proc Natl Acad Sci U S A 102(50):18165-70. Cerca con Google

Shirvalkar PR, Rapp PR, Shapiro ML. 2010. Bidirectional changes to hippocampal theta-gamma comodulation predict memory for recent spatial episodes. Proc Natl Acad Sci U S A 107(15):7054-9. Cerca con Google

Smith SJ. 2005. EEG in neurological conditions other than epilepsy: When does it help, what does it add? J Neurol Neurosurg Psychiatry 76 Suppl 2:ii8-12. Cerca con Google

Sperling R and Johnson K. 2013a. Biomarkers of alzheimer disease: Current and future applications to diagnostic criteria. CONTINUUM: Lifelong Learning in Neurology 19(2, Dementia):325-38. Cerca con Google

Sperling R, Mormino E, Johnson K. 2014. The evolution of preclinical alzheimer's disease: Implications for prevention trials. Neuron 84(3):608-22. Cerca con Google

Sperling RA, LaViolette PS, O'Keefe K, O'Brien J, Rentz DM, Pihlajamaki M, Marshall G, Hyman BT, Selkoe DJ, Hedden T. 2009. Amyloid deposition is associated with impaired default network function in older persons without dementia. Neuron 63(2):178-88. Cerca con Google

Sperling R and Johnson K. 2013b. Biomarkers of alzheimer disease: Current and future applications to diagnostic criteria. Continuum (Minneap Minn) 19(2 Dementia):325-38. Cerca con Google

Sporns O. 2011. Networks of the brain. MIT press. Cerca con Google

Squire LR, Stark CE, Clark RE. 2004. The medial temporal lobe*. Annu Rev Neurosci 27:279-306. Cerca con Google

Stargardt A, Swaab DF, Bossers K. 2015. The storm before the quiet: Neuronal hyperactivity and aß in the presymptomatic stages of alzheimer's disease. Neurobiol Aging 36(1):1-11. Cerca con Google

Steardo Jr L, Bronzuoli MR, Iacomino A, Esposito G, Steardo L, Scuderi C. 2015. Does neuroinflammation turn on the flame in alzheimer's disease? focus on astrocytes. Frontiers in Neuroscience 9. Cerca con Google

Steriade M and Deschenes M. 1984. The thalamus as a neuronal oscillator. Brain Res Rev 8(1):1-63. Cerca con Google

Steriade M, Gloor P, Llinas R, Da Silva FL, Mesulam M. 1990. Basic mechanisms of cerebral rhythmic activities. Electroencephalogr Clin Neurophysiol 76(6):481-508. Cerca con Google

Steriade M, Nunez A, Amzica F. 1993. A novel slow (< 1 hz) oscillation of neocortical neurons in vivo: Depolarizing and hyperpolarizing components. J Neurosci 13(8):3252-65. Cerca con Google

Strozyk D, Blennow K, White LR, Launer LJ. 2003. CSF abeta 42 levels correlate with amyloid-neuropathology in a population-based autopsy study. Neurology 60(4):652-6. Cerca con Google

Sturchler-Pierrat C, Abramowski D, Duke M, Wiederhold KH, Mistl C, Rothacher S, Ledermann B, Burki K, Frey P, Paganetti PA, et al. 1997. Two amyloid precursor protein transgenic mouse models with alzheimer disease-like pathology. Proc Natl Acad Sci U S A 94(24):13287-92. Cerca con Google

Stutzmann GE, Caccamo A, LaFerla FM, Parker I. 2004. Dysregulated IP3 signaling in cortical neurons of knock-in mice expressing an alzheimer's-linked mutation in presenilin1 results in exaggerated Ca2+ signals and altered membrane excitability. J Neurosci 24(2):508-13. Cerca con Google

Stutzmann GE, Smith I, Caccamo A, Oddo S, Laferla FM, Parker I. 2006. Enhanced ryanodine receptor recruitment contributes to Ca2+ disruptions in young, adult, and aged alzheimer's disease mice. J Neurosci 26(19):5180-9. Cerca con Google

Suzuki N, Cheung TT, Cai XD, Odaka A, Otvos L,Jr, Eckman C, Golde TE, Younkin SG. 1994. An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants. Science 264(5163):1336-40. Cerca con Google

Tanila J., Minkeviciene R. and Dobszay MB. 2008. Fibrillar beta-amyloid associates with epileptic seizures in APPswe/PS1de9 mice and changes excitability in cortical and hippocampal neurons. Society for neuroscience annual meeting. Cerca con Google

Terry RD, Masliah E, Salmon DP, Butters N, DeTeresa R, Hill R, Hansen LA, Katzman R. 1991. Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment. Ann Neurol 30(4):572-80. Cerca con Google

Tomiyama T, Nagata T, Shimada H, Teraoka R, Fukushima A, Kanemitsu H, Takuma H, Kuwano R, Imagawa M, Ataka S. 2008. A new amyloid ß variant favoring oligomerization in alzheimer's' type dementia. Ann Neurol 63(3):377-87. Cerca con Google

Tomlinson B, Blessed G, Roth M. 1970. Observations on the brains of demented old people. J Neurol Sci 11(3):205-42. Cerca con Google

Tort AB, Komorowski R, Eichenbaum H, Kopell N. 2010. Measuring phase-amplitude coupling between neuronal oscillations of different frequencies. J Neurophysiol 104(2):1195-210. Cerca con Google

Tort AB, Komorowski RW, Manns JR, Kopell NJ, Eichenbaum H. 2009. Theta' gamma coupling increases during the learning of item' context associations. Proceedings of the National Academy of Sciences 106(49):20942-7. Cerca con Google

Trambaiolli LR, Lorena AC, Fraga FJ, Kanda PA, Anghinah R, Nitrini R. 2011. Improving alzheimer's disease diagnosis with machine learning techniques. Clin EEG Neurosci 42(3):160-5. Cerca con Google

Tu H, Nelson O, Bezprozvanny A, Wang Z, Lee S, Hao Y, Serneels L, De Strooper B, Yu G, Bezprozvanny I. 2006. Presenilins form ER ca 2 leak channels, a function disrupted by familial alzheimer's disease-linked mutations. Cell 126(5):981-93. Cerca con Google

Van Vugt MK, Schulze-Bonhage A, Litt B, Brandt A, Kahana MJ. 2010. Hippocampal gamma oscillations increase with memory load. The Journal of Neuroscience 30(7):2694-9. Cerca con Google

Vandecasteele M, Varga V, Berenyi A, Papp E, Bartho P, Venance L, Freund TF, Buzsaki G. 2014. Optogenetic activation of septal cholinergic neurons suppresses sharp wave ripples and enhances theta oscillations in the hippocampus. Proc Natl Acad Sci U S A 111(37):13535-40. Cerca con Google

Vanderwolf CH. 1969. Hippocampal electrical activity and voluntary movement in the rat. Electroencephalogr Clin Neurophysiol 26(4):407-18. Cerca con Google

Vanderwolf C. 2001. The hippocampus as an olfacto-motor mechanism: Were the classical anatomists right after all? Behav Brain Res 127(1):25-47. Cerca con Google

Verret L, Mann EO, Hang GB, Barth AM, Cobos I, Ho K, Devidze N, Masliah E, Kreitzer AC, Mody I. 2012. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in alzheimer model. Cell 149(3):708-21. Cerca con Google

Vidal M, Morris R, Grosveld F, Spanopoulou E. 1990. Tissue-specific control elements of the thy-1 gene. Embo J 9(3):833-40. Cerca con Google

Villemagne VL, Burnham S, Bourgeat P, Brown B, Ellis KA, Salvado O, Szoeke C, Macaulay SL, Martins R, Maruff P. 2013. Amyloid ß deposition, neurodegeneration, and cognitive decline in sporadic alzheimer's disease: A prospective cohort study. The Lancet Neurology 12(4):357-67. Cerca con Google

Voytek B and Knight RT. 2015. Dynamic network communication as a unifying neural basis for cognition, development, aging, and disease. Biol Psychiatry 77(12):1089-97. Cerca con Google

Voytek B, Kramer MA, Case J, Lepage KQ, Tempesta ZR, Knight RT, Gazzaley A. 2015. Age-related changes in 1/f neural electrophysiological noise. J Neurosci 35(38):13257-65. Cerca con Google

Wang Z, Tan L, Liu J, Yu J. 2015. The essential role of soluble aß oligomers in alzheimer's disease. Mol Neurobiol :1-20. Cerca con Google

Webster SJ, Bachstetter AD, Nelson PT, Schmitt FA, Van Eldik LJ. 2014. Using mice to model alzheimer's dementia: An overview of the clinical disease and the preclinical behavioral changes in 10 mouse models. Frontiers in Genetics 5. Cerca con Google

Westmark CJ, Westmark PR, Beard AM, Hildebrandt SM, Malter JS. 2008. Seizure susceptibility and mortality in mice that over-express amyloid precursor protein. Int J Clin Exp Pathol 1(2):157-68. Cerca con Google

Winson J. 1978. Loss of hippocampal theta rhythm results in spatial memory deficit in the rat. Science 201(4351):160-3. Cerca con Google

Wirths O, Multhaup G, Czech C, Blanchard V, Moussaoui S, Tremp G, Pradier L, Beyreuther K, Bayer TA. 2001. Intraneuronal aß accumulation precedes plaque formation in ß-amyloid precursor protein and presenilin-1 double-transgenic mice. Neurosci Lett 306(1):116-20. Cerca con Google

Wolansky T, Clement EA, Peters SR, Palczak MA, Dickson CT. 2006. Hippocampal slow oscillation: A novel EEG state and its coordination with ongoing neocortical activity. J Neurosci 26(23):6213-29. Cerca con Google

World Health Organization,. 2015. Fact sheet N'°362, march 2015. . Cerca con Google

Yanovsky Y, Ciatipis M, Draguhn A, Tort AB, Brankack J. 2014. Slow oscillations in the mouse hippocampus entrained by nasal respiration. J Neurosci 34(17):5949-64. Cerca con Google

Younkin SG. 1995. Evidence that Aß42 is the real culprit in alzheimer's disease. Ann Neurol 37(3):287-8. Cerca con Google

Yuk DY, Lee YK, Nam SY, Yun YW, Hwang DY, Choi DY, Oh KW, Hong JT. 2009. Reduced anxiety in the mice expressing mutant (N141I) presenilin 2. J Neurosci Res 87(2):522-31. Cerca con Google

Zahs KR and Ashe KH. 2010. 'Too much good news' are alzheimer mouse models trying to tell us how to prevent, not cure, alzheimer's disease? Trends Neurosci 33(8):381-9. Cerca con Google

Zampese E, Fasolato C, Pozzan T, Pizzo P. 2011a. Presenilin-2 modulation of ER-mitochondria interactions: FAD mutations, mechanisms and pathological consequences. Communicative & Integrative Biology 4(3):357-60. Cerca con Google

Zampese E, Fasolato C, Kipanyula MJ, Bortolozzi M, Pozzan T, Pizzo P. 2011b. Presenilin 2 modulates endoplasmic reticulum (ER)-mitochondria interactions and Ca2+ cross-talk. Proc Natl Acad Sci U S A 108(7):2777-82. Cerca con Google

Zatti G, Burgo A, Giacomello M, Barbiero L, Ghidoni R, Sinigaglia G, Florean C, Bagnoli S, Binetti G, Sorbi S. 2006. Presenilin mutations linked to familial alzheimer's disease reduce endoplasmic reticulum and golgi apparatus calcium levels. Cell Calcium 39(6):539-50. Cerca con Google

Zeineh MM, Engel SA, Thompson PM, Bookheimer SY. 2003. Dynamics of the hippocampus during encoding and retrieval of face-name pairs. Science 299(5606):577-80. Cerca con Google

Zetterberg H, Tullhog K, Hansson O, Minthon L, Londos E, Blennow K. 2010. Low incidence of post-lumbar puncture headache in 1,089 consecutive memory clinic patients. Eur Neurol 63(6):326-30. Cerca con Google

Zhang C, Wang H, Wang H, Wu M. 2013. EEG-based expert system using complexity measures and probability density function control in alpha sub-band. Integrated Computer-Aided Engineering 20(4):391-405. Cerca con Google

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