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High-quality sleep alleviates cognitive deficits linked to genetic risk for Alzheimer’s disease in older African Americans

The study sheds light on the importance of sleep in reducing the risk of cognitive decline in this vulnerable population.

In a study focused on the interplay between sleep and genetic factors associated with Alzheimer’s disease (AD) in older African Americans, researchers have discovered that high-quality sleep may mitigate cognitive deficits related to the ABCA7 gene.

The study sheds light on the importance of sleep in reducing the risk of cognitive decline in this vulnerable population.

“This new finding suggests that someone with a high-risk variant might be able to overcome their genetic inheritance by improving their sleep habits,” Bernadette Fausto, a member of the research faculty at Rutgers University-Newark in New Jersey, said in a news release. “The findings were striking.”

The findings, published in the latest issue of The Journal of Alzheimer’s Disease, highlighted the disproportionate impact of both sleep deficiencies and AD on older African Americans.

Furthermore, genetic susceptibility to AD, particularly the ABCA7 rs115550680 locus, compounds the risk for cognitive decline among individuals in this group.

The study’s goal was to look at how the quality of sleep and the ABCA7 rs115550680 gene variant affect cognitive function.

The study focused on hippocampal-dependent cognitive tasks closely linked to AD, and involved 114 cognitively healthy older African Americans genotyped for ABCA7 risk.

Of the participants, 57 were carriers of the risk ‘G’ allele, while the remaining 57 were non-carriers.

The participants completed lifestyle questionnaires, underwent cognitive assessments, and provided self-reported sleep quality ratings (poor, average, good).

Age and years of education were considered covariates in the analysis.

The results obtained through analysis of covariance (ANCOVA) revealed a significant interaction between the ABCA7 risk genotype and sleep quality.

Carriers of the risk genotype who reported poor or average sleep quality exhibited markedly poorer generalization of prior learning (a cognitive marker of AD) compared to their non-risk counterparts.

In contrast, no genotype-related difference in generalization performance was observed among individuals who reported good sleep quality.

“These findings suggest that high-quality sleep may have a neuro-protective effect against the genetic risk for Alzheimer’s disease,” the researchers wrote. “Improving sleep quality could potentially be an effective strategy in reducing cognitive decline in older African Americans.”

Researchers said the study’s conclusions underscored the need for further investigation into how sleep affects the pathogenesis and progression of AD associated with the ABCA7 gene.

The researchers concluded that future studies employing more rigorous methodology and examining sleep neurophysiology are warranted to elucidate the specific role of sleep in AD development.

Further, they emphasize the importance of developing non-invasive sleep interventions tailored to racial groups, considering their specific genetic risk profiles for AD.

“Such interventions could prove crucial in mitigating the cognitive impact of genetic susceptibility in older African Americans and reducing health disparities in AD,” the study found.

Researchers determined that, as the scientific community gains a deeper understanding of the complex relationship between sleep, genetics, and cognitive function, the findings may pave the way for novel approaches to prevent or delay the onset of Alzheimer’s disease in vulnerable populations, ultimately improving the overall well-being of older African Americans.

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