ABCA2 is a strong genetic risk factor for early-onset Alzheimer's disease

2005 ◽  
Vol 18 (1) ◽  
pp. 119-125 ◽  
Author(s):  
Sandrine Macé ◽  
Emmanuelle Cousin ◽  
Sylvain Ricard ◽  
Emmanuelle Génin ◽  
Emmanuel Spanakis ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Genetic Risk ◽  
Early Onset ◽  
Genetic Risk Factor ◽  
Early Onset Alzheimer’S Disease

O1-04-06: Elevated cerebrospinal fluid amyloid-Beta42 levels in young adults at genetic risk for early-onset alzheimer's disease

2011 ◽  
Vol 7 ◽  
pp. S102-S103 ◽  
Author(s):  
Eric Reiman ◽  
Carlos Velez-Pardo ◽  
Marelene Jimenez del Rio ◽  
Margarita Giraldo ◽  
Natalia Acosta-Baena ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Young Adults ◽  
Genetic Risk ◽  
Early Onset ◽  
Early Onset Alzheimer’S Disease

scholarly journals ApoE4 attenuates cortical neuronal activity and impairs memory in young apoE4 rats

2021 ◽  
Author(s):  
Ilona Har-Paz ◽  
Elor Arieli ◽  
Anan Moran
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Neuronal Activity ◽  
Genetic Risk ◽  
Cortical Neurons ◽  
Late Onset ◽  
Genetic Risk Factor ◽  
Normal Brain ◽  
Brain Functions

AbstractThe E4 allele of apolipoprotein E (apoE4) is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD). However, apoE4 may cause innate brain abnormalities before the appearance of AD related neuropathology. Understanding these primary dysfunctions is vital for early detection of AD and the development of therapeutic strategies for it. Recently we have shown impaired extra-hippocampal memory in young apoE4 mice – a deficit that was correlated with attenuated structural pre-synaptic plasticity in cortical and subcortical regions. Here we test the hypothesis that these early structural deficits impact learning via changes in basal and stimuli evoked neuronal activity. We recorded extracellular neuronal activity from the gustatory cortex (GC) of three-month-old humanized apoE4 and wildtype rats, before and after conditioned taste aversion (CTA) training. Despite normal sucrose drinking behavior before CTA, young apoE4 rats showed impaired CTA learning, consistent with our previous results in apoE4 mice. This behavioral deficit was correlated with decreased basal and taste-evoked firing rates in both putative excitatory and inhibitory GC neurons. Single neuron and ensemble analyses of taste coding demonstrated that apoE4 neurons could be used to correctly classify tastes, but were unable to undergo plasticity to support learning. Our results suggest that apoE4 impacts brain excitability and plasticity early in life and may act as an initiator for later AD pathologies.Significant statementThe ApoE4 allele is the strongest genetic risk-factor for late-onset Alzheimer’s disease (AD), yet the link between apoE4 and AD is still unclear. Recent molecular and in-vitro studies suggest that apoE4 interferes with normal brain functions decades before the development of its related AD neuropathology. Here we recorded the activity of cortical neurons from young apoE4 rats during extra-hippocampal learning to study early apoE4 neuronal activity abnormalities, and their effects over coding capacities. We show that apoE4 drastically reduces basal and stimuli-evoked cortical activity in both excitatory and inhibitory neurons. The apoE4-induced activity attenuation did not prevent coding of stimuli identity and valence, but impaired capacity to undergo activity changes to support learning. Our findings support the hypothesis that apoE4 interfere with normal neuronal plasticity early in life; a deficit that may lead to late-onset AD development.

scholarly journals Elucidating Molecular Phenotypes Caused by the SORL1 Alzheimer’s Disease Genetic Risk Factor Using Human Induced Pluripotent Stem Cells

2015 ◽  
Vol 16 (4) ◽  
pp. 373-385 ◽  
Author(s):  
Jessica E. Young ◽  
Jonathan Boulanger-Weill ◽  
Daniel A. Williams ◽  
Grace Woodruff ◽  
Floyd Buen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Risk Factor ◽  
Induced Pluripotent Stem Cells ◽  
Pluripotent Stem Cells ◽  
Genetic Risk ◽  
Genetic Risk Factor ◽  
Induced Pluripotent ◽  
Molecular Phenotypes

scholarly journals IC-P-066: Task-dependent fMRI abnormalities in young adults at genetic risk for early-onset Alzheimer's disease

2011 ◽  
Vol 7 ◽  
pp. S34-S35
Author(s):  
Yakeel Quiroz ◽  
Reisa Sperling ◽  
Francisco Lopera ◽  
Adam Fleisher ◽  
Kewei Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Young Adults ◽  
Genetic Risk ◽  
Early Onset ◽  
Early Onset Alzheimer’S Disease

Is HCRTR2 a Genetic Risk Factor for Alzheimer's Disease?

2014 ◽  
Vol 38 (3-4) ◽  
pp. 245-253 ◽  
Author(s):  
Salvatore Gallone ◽  
Silvia Boschi ◽  
Elisa Rubino ◽  
Paola De Martino ◽  
Elio Scarpini ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Genetic Risk ◽  
Genetic Risk Factor

scholarly journals Probability Model of Allele Frequency of Alzheimer’s Disease Genetic Risk Factor

2016 ◽  
Vol 4 (2) ◽  
pp. 43-48
Author(s):  
Afshin Fayyaz-Movaghar ◽  
Mohammad Taghi Kamel-Mirmostafaee ◽  
Tahura Sadat Borhani ◽  
◽  
◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Allele Frequency ◽  
Genetic Risk ◽  
Probability Model ◽  
Genetic Risk Factor

scholarly journals Analysis of Causative Genes and Genetic Risk Factor in Alzheimer's Disease.

2001 ◽  
Vol 38 (6) ◽  
pp. 769-771 ◽  
Author(s):  
Katsuya Urakami ◽  
Yosuke Wakutani ◽  
Kenji Wada-Isoe ◽  
Kaoru Yamagata ◽  
Yoshiki Adachi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Genetic Risk ◽  
Genetic Risk Factor

P1-374: Reduced regional gray matter in cognitively normal young adults at genetic risk for early-onset Alzheimer's disease

2011 ◽  
Vol 7 ◽  
pp. S232-S232 ◽  
Author(s):  
Adam Fleisher ◽  
Yakeel Quiroz ◽  
Kewei Chen ◽  
Jessica Langbaum ◽  
Pradeep Thiyyagura ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Young Adults ◽  
Gray Matter ◽  
Genetic Risk ◽  
Early Onset ◽  
Cognitively Normal ◽  
Early Onset Alzheimer’S Disease
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