Alzheimer's Genetic Risk; Underreported Dementia; Exercise or Nap After Sleep Loss?
(MedPage Today) -- A new APOE-independent multi-ancestry polygenic risk score for Alzheimer's disease was associated with cognitive decline and neuropathological hallmarks in a study of diverse populations. (Nature Genetics) Diabetes-related cortical...
Researchers have developed a new genetic risk score for Alzheimer's disease that works regardless of the APOE gene, which previously held a central role in Alzheimer's risk. This multi-ancestry polygenic risk score was found to be linked to cognitive decline and certain hallmark signs in the brain's neuropathology across various populations.
While this genetic risk score is promising, Alzheimer's diagnosis remains underreported. In fact, 67% of participants with a claims-based dementia diagnosis did not self-report their diagnosis, a finding that significantly surpasses the underreporting rates seen in other health conditions. This highlights the need for better awareness and reporting of Alzheimer's disease.
The relationship between depression and cognitive decline is complex and may be influenced by chronic exposure to adverse policing experiences. A study of older Black adults in the U.S. found that such chronic exposure could affect how depressive symptoms impact cognitive function.
In the realm of dementia-related brain pathology, a study using imaging data revealed that diabetes-related cortical thinning in cognitively unimpaired older adults followed a unique regional pattern. This pattern was distinct from Alzheimer's and cerebrovascular pathology, suggesting a new area of focus in understanding diabetes-related cognitive decline.
The use of amyloid-targeting therapies in Alzheimer's patients with suspected co-pathologies, such as cerebrovascular disease or Lewy body dementia, requires careful clinical judgment. Researchers emphasized the necessity of shared decision-making between patients and healthcare providers when considering these therapies.
Two phase III trials conducted by Novartis provided additional insights. The oral Bruton's tyrosine kinase inhibitor remibrutinib (Rhapsido) reduced relapse rates in patients with chronic spontaneous urticaria compared to teriflunomide (Aubagio). This trial demonstrates the potential of a new drug class in managing chronic conditions.
In a large prospective cohort study, older adults who experienced food insecurity in midlife and late life had higher risks of probable dementia. This finding underscores the importance of addressing social determinants of health, such as food insecurity, in the prevention and management of dementia.
Interestingly, both exercise and napping were found to protect episodic memory after sleep loss. However, these interventions used distinct brain mechanisms. Exercise primarily activated regions involved in attention and executive function, while napping engaged areas associated with memory consolidation. These findings suggest that older adults experiencing sleep loss can employ various strategies to preserve their memory function.
In a study analyzing brain donors, only 31% of former National Football League players with clinician-adjudicated dementia had neurodegenerative disease listed as their underlying cause of death. This finding highlights the underreporting of neurodegenerative diseases, particularly in athletes, and advocates for more accurate and comprehensive death certificates.
Lastly, a groundbreaking map of proteins linked to autism has been unveiled. This comprehensive resource provides researchers with a wealth of information to further unravel the genetic and molecular underpinnings of autism spectrum disorder. With this new map, scientists can identify key players in the pathogenesis of autism and develop targeted therapeutic strategies.
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