Impact of APOE and BDNF Val66Met gene polymorphisms on cognitive functions in patients with amnestic mild cognitive impairment

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F20%3A10395817" target="_blank" >RIV/00216208:11130/20:10395817 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00159816:_____/20:00072945 RIV/00064203:_____/20:10395817 RIV/00023884:_____/20:00008702

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=Xi7NbsQKQ6" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=Xi7NbsQKQ6</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3233/JAD-190464" target="_blank" >10.3233/JAD-190464</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Impact of APOE and BDNF Val66Met gene polymorphisms on cognitive functions in patients with amnestic mild cognitive impairment

Popis výsledku v původním jazyce

Apolipoprotein (APOE) ε4 is a well-known risk factor for late-onset Alzheimer disease (AD), but other AD-related gene polymorphisms might also be important, such as polymorphisms within the brain-derived neurotrophic factor (BDNF) gene. Carriage of BDNF Val66Met has been associated with faster cognitive decline and greater hippocampal atrophy in cognitively normal elderly. We examined the effects of the concurrent presence of APOE and BDNF polymorphisms on cognitive functions and brain morphometry in amnestic mild cognitive impairment (aMCI) patients. 107 aMCI patients (mean age=72.2) were recruited from the Czech Brain Aging Study and based on APOE and BDNF genes polymorphisms were into 4 groups: ε4-BDNFVal/Val (n=37), ε4-BDNFMet (n=19), ε4+BDNFVal/Val (n=35), ε4+BDNFMet (n=16). All patients underwent clinical examination, magnetic resonance imaging and complex neuropsychological battery. Among BDNFMet carriers, we observed that APOE 4+ carriers performed worse than APOE 3 homozygotes in immediate and delayed recall. There was no difference in memory performance associated with APOE variation in BDNFVal homozygotes. We did not observe increased atrophy in areas related to memory function in the ε4+BDNFMet group. Our findings suggest that carriage of ε4+BDNFMet is associated with more pronounced memory dysfunction, which is typical feature for early AD, but not with structural brain changes in aMCI patients. These findings suggest that in APOE ε4/BDNF Met carriers, synaptic dysfunction affecting memory may precede pronounced structural changes.

Název v anglickém jazyce

Impact of APOE and BDNF Val66Met gene polymorphisms on cognitive functions in patients with amnestic mild cognitive impairment

Popis výsledku anglicky

Apolipoprotein (APOE) ε4 is a well-known risk factor for late-onset Alzheimer disease (AD), but other AD-related gene polymorphisms might also be important, such as polymorphisms within the brain-derived neurotrophic factor (BDNF) gene. Carriage of BDNF Val66Met has been associated with faster cognitive decline and greater hippocampal atrophy in cognitively normal elderly. We examined the effects of the concurrent presence of APOE and BDNF polymorphisms on cognitive functions and brain morphometry in amnestic mild cognitive impairment (aMCI) patients. 107 aMCI patients (mean age=72.2) were recruited from the Czech Brain Aging Study and based on APOE and BDNF genes polymorphisms were into 4 groups: ε4-BDNFVal/Val (n=37), ε4-BDNFMet (n=19), ε4+BDNFVal/Val (n=35), ε4+BDNFMet (n=16). All patients underwent clinical examination, magnetic resonance imaging and complex neuropsychological battery. Among BDNFMet carriers, we observed that APOE 4+ carriers performed worse than APOE 3 homozygotes in immediate and delayed recall. There was no difference in memory performance associated with APOE variation in BDNFVal homozygotes. We did not observe increased atrophy in areas related to memory function in the ε4+BDNFMet group. Our findings suggest that carriage of ε4+BDNFMet is associated with more pronounced memory dysfunction, which is typical feature for early AD, but not with structural brain changes in aMCI patients. These findings suggest that in APOE ε4/BDNF Met carriers, synaptic dysfunction affecting memory may precede pronounced structural changes.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30103 - Neurosciences (including psychophysiology)

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2020

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Alzheimer&apos;s Disease

ISSN

1387-2877

e-ISSN

—

Svazek periodika

73

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

11

Strana od-do

247-257

Kód UT WoS článku

000506311500020

EID výsledku v databázi Scopus

2-s2.0-85077802085