According to the National Institute on Aging, the Alzheimer’s Association, and other researchers, Black Americans are approximately twice as likely as white Americans to develop dementia and Alzheimer’s. The reasons for this disparity are unknown — perhaps in part because Black individuals are much less likely than whites to participate in Alzheimer’s and dementia research studies.
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New findings reveal a subtle but powerful breakdown that may help explain early memory loss in Alzheimer’s.
When the brain rests, it usually replays recent experiences to strengthen memory. Scientists found that in Alzheimer’s-like mice, this replay still occurs — but the signals are jumbled and poorly coordinated. As a result, memory-supporting brain cells lose their stability, and the animals struggle to remember where they’ve been.
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Scientists have found a potential new way to slow memory loss in Alzheimer’s, a neurodegenerative disorder that gradually damages memory and thinking, according to a new study.
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Scientists at Tokyo Metropolitan University have turned to polymer physics to better understand one of the defining features of Alzheimer’s disease: the formation of tau protein fibrils. Their research shows that these fibrils do not form directly. Instead, tau proteins first gather into large clusters, similar to how polymers begin to crystallize. When researchers disrupted these early clusters, fibrils failed to develop in solution.
This finding points to a major shift in how future treatments for neurodegenerative diseases might be designed.
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Sleep duration and quality may be associated with fluid biomarkers present in Alzheimer disease, wrote authors of a systematic review published in Sleep Medicine Reviews. Specifically, short sleep duration was associated with higher levels of Alzheimer disease–related biomarkers.
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Chlamydia pneumoniae—a common bacterium that causes pneumonia and sinus infections—can linger in the eye and brain for years and may aggravate Alzheimer’s disease, according to a study from Cedars-Sinai. Published in Nature Communications, the discovery suggests this bacterium can amplify Alzheimer’s disease and points to potential interventions including inflammation-limiting therapies and early antibiotic treatment.
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