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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. [Ph.D. thesis]

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Abstract (italian or english)

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 (a different language)

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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EPrint type:Ph.D. thesis
Tutor:Fasolato, Cristina
Data di deposito della tesi:01 February 2016
Anno di Pubblicazione:01 February 2016
Key Words: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 Oct 2016 10:25
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