scholarly journals The Histone H3 K4me3, K27me3, and K27ac Genome-Wide Distributions Are Differently Influenced by Sex in Brain Cortexes and Gastrocnemius of the Alzheimer’s Disease PSAPP Mouse Model

Epigenomes ◽  
2021 ◽  
Vol 5 (4) ◽  
pp. 26
Author(s):  
Francesca Casciaro ◽  
Giuseppe Persico ◽  
Martina Rusin ◽  
Stefano Amatori ◽  
Claire Montgomery ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Mouse Model ◽  
Histone H3 ◽  
Signal Distribution ◽  
Dementia Prevalence ◽  
Genome Wide ◽  
Gastrocnemius Muscles ◽  
Behavioral Mechanisms

Background: Women represent the majority of Alzheimer’s disease patients and show typical symptoms. Genetic, hormonal, and behavioral mechanisms have been proposed to explain sex differences in dementia prevalence. However, whether sex differences exist in the epigenetic landscape of neuronal tissue during the progression of the disease is still unknown. Methods: To investigate the differences of histone H3 modifications involved in transcription, we determined the genome-wide profiles of H3K4me3, H3K27ac, and H3K27me3 in brain cortexes of an Alzheimer mouse model (PSAPP). Gastrocnemius muscles were also tested since they are known to be different in the two sexes and are affected during the disease progression. Results: Correlation analysis distinguished the samples based on sex for H3K4me3 and H3K27me3 but not for H3K27ac. The analysis of transcription starting sites (TSS) signal distribution, and analysis of bounding sites revealed that gastrocnemius is more influenced than brain by sex for the three histone modifications considered, exception made for H3K27me3 distribution on the X chromosome which showed sex-related differences in promoters belonging to behavior and cellular or neuronal spheres in mice cortexes. Conclusions: H3K4me3, H3K27ac, and H3K27me3 signals are slightly affected by sex in brain, with the exception of H3K27me3, while a higher number of differences can be found in gastrocnemius.

Sex differences in response to a high fat diet in an Alzheimer’s Disease mouse model

2018 ◽  
Author(s):  
Alejandra Freire Fernández-Regatillo ◽  
María L. de Ceballos ◽  
Jesús Argente ◽  
Sonia Díaz Pacheco ◽  
Clara González Martínez
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Mouse Model ◽  
High Fat Diet ◽  
High Fat

scholarly journals Sex Differences in Healthspan Predict Lifespan in the 3xTg-AD Mouse Model of Alzheimer’s Disease

2018 ◽  
Vol 10 ◽  
Author(s):  
Alice E. Kane ◽  
Sooyoun Shin ◽  
Aimee A. Wong ◽  
Emre Fertan ◽  
Natalia S. Faustova ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

scholarly journals Genome-wide alteration of 5-hydroxymenthylcytosine in a mouse model of Alzheimer’s disease

BMC Genomics ◽  
2016 ◽  
Vol 17 (1) ◽  
Author(s):  
Liqi Shu ◽  
Wenjia Sun ◽  
Liping Li ◽  
Zihui Xu ◽  
Li Lin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Genome Wide

Sex Differences in Cognition, Neuropsychiatric Symptoms, and Sleep in an Alzheimer’s Disease Mouse Model

2021 ◽  
Vol 89 (9) ◽  
pp. S116
Author(s):  
Holly Hunsberger ◽  
Seonjoo Lee ◽  
Alicia Whye ◽  
Keerthana Jayaseelan ◽  
Miranda Scarlata ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Mouse Model ◽  
Neuropsychiatric Symptoms

scholarly journals Genome-Wide Analysis of miRNA Signature in the APPswe/PS1ΔE9 Mouse Model of Alzheimer's Disease

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e101725 ◽  
Author(s):  
Hongxue Luo ◽  
Qi Wu ◽  
Xiaoyang Ye ◽  
Yi Xiong ◽  
Jinyong Zhu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Mirna Signature ◽  
Genome Wide Analysis ◽  
Model Of Alzheimer’S Disease ◽  
Genome Wide

scholarly journals Genome-wide profiling reveals functional diversification of ∆FosB gene targets in the hippocampus of an Alzheimer's disease mouse model

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0192508 ◽  
Author(s):  
Jason C. You ◽  
Gabriel S. Stephens ◽  
Chia-Hsuan Fu ◽  
Xiaohong Zhang ◽  
Yin Liu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Functional Diversification ◽  
Genome Wide

scholarly journals Sex differences in the genetic predictors of Alzheimer’s pathology

Brain ◽  
2019 ◽  
Vol 142 (9) ◽  
pp. 2581-2589 ◽  
Author(s):  
Logan Dumitrescu ◽  
Lisa L Barnes ◽  
Madhav Thambisetty ◽  
Gary Beecham ◽  
Brian Kunkle ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Disease Risk ◽  
Association Studies ◽  
Age At Onset ◽  
Genome Wide Association Studies ◽  
Genetic Associations ◽  
Data Repositories ◽  
Genome Wide

Abstract Autopsy measures of Alzheimer’s disease neuropathology have been leveraged as endophenotypes in previous genome-wide association studies (GWAS). However, despite evidence of sex differences in Alzheimer’s disease risk, sex-stratified models have not been incorporated into previous GWAS analyses. We looked for sex-specific genetic associations with Alzheimer’s disease endophenotypes from six brain bank data repositories. The pooled dataset included 2701 males and 3275 females, the majority of whom were diagnosed with Alzheimer’s disease at autopsy (70%). Sex-stratified GWAS were performed within each dataset and then meta-analysed. Loci that reached genome-wide significance (P < 5 × 10−8) in stratified models were further assessed for sex interactions. Additional analyses were performed in independent datasets leveraging cognitive, neuroimaging and CSF endophenotypes, along with age-at-onset data. Outside of the APOE region, one locus on chromosome 7 (rs34331204) showed a sex-specific association with neurofibrillary tangles among males (P = 2.5 × 10−8) but not females (P = 0.85, sex-interaction P = 2.9 × 10−4). In follow-up analyses, rs34331204 was also associated with hippocampal volume, executive function, and age-at-onset only among males. These results implicate a novel locus that confers male-specific protection from tau pathology and highlight the value of assessing genetic associations in a sex-specific manner.

scholarly journals Sex Differences in a Novel Triple Knock‐in Mouse Model of Alzheimer's Disease

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Cedrick M Daphney ◽  
Neha Milind Chitre ◽  
Melissa M Milfort ◽  
Kevin Sean Murnane
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease

scholarly journals Similar Genetic Architecture of Alzheimer’s Disease and Differential APOE Effect Between Sexes

2021 ◽  
Vol 13 ◽  
Author(s):  
Hao Wang ◽  
Min-Tzu Lo ◽  
Sara Brin Rosenthal ◽  
Carolina Makowski ◽  
Ole A. Andreassen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Genetic Correlation ◽  
Genetic Architecture ◽  
Clinical Manifestations ◽  
Genome Wide ◽  
Significant Locus ◽  
Active Research ◽  
Or Gene

Sex differences have been observed in the clinical manifestations of Alzheimer’s disease (AD) and elucidating their genetic basis is an active research topic. Based on autosomal genotype data of 7,216 men and 10,680 women, including 8,136 AD cases and 9,760 controls, we explored sex-related genetic heterogeneity in AD by investigating SNP heritability, genetic correlation, as well as SNP- and gene-based genome-wide analyses. We found similar SNP heritability (men: 19.5%; women: 21.5%) and high genetic correlation (Rg = 0.96) between the sexes. The heritability of APOE ε4-related risks for AD, after accounting for effects of all SNPs excluding chromosome 19, was nominally, but not significantly, higher in women (10.6%) than men (9.7%). In age-stratified analyses, ε3/ε4 was associated with a higher risk of AD among women than men aged 65–75 years, but not in the full sample. Apart from APOE, no new significant locus was identified in sex-stratified gene-based analyses. Our result of the high genetic correlation indicates overall similar genetic architecture of AD in both sexes at the genome-wide averaged level. Our study suggests that clinically observed sex differences may arise from sex-specific variants with small effects or more complicated mechanisms involving epigenetic alterations, sex chromosomes, or gene-environment interactions.

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