Alzheimer's
Study links tanycyte damage to reduced tau clearance in Alzheimer’s disease
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Researchers report that tanycytes—specialized cells lining the brain’s third ventricle—can help move tau protein from cerebrospinal fluid into the bloodstream, and that signs of tanycyte disruption in Alzheimer’s patient tissue may be associated with impaired tau removal. The findings, published March 5 in Cell Press Blue, are based on animal and cell experiments and analyses of human brain samples.
Researchers at Scripps Research have developed a blood test that detects Alzheimer's disease by analyzing structural changes in blood proteins. The method identifies differences in three specific proteins, allowing accurate distinction between healthy individuals, those with mild cognitive impairment, and Alzheimer's patients. Published in Nature Aging on February 27, 2026, the findings could enable earlier diagnosis and treatment.
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Building on genomic research linking Alzheimer's origins to inflammation in peripheral tissues like the gut, lungs, or skin, practical lifestyle measures can help curb chronic inflammation. These include vaccination, oral hygiene, diet, exercise, weight control, and stress management, offering benefits for overall health amid evolving science.
Researchers at Sweden’s Karolinska Institutet and Japan’s RIKEN Center for Brain Science report that two somatostatin receptors, SST1 and SST4, jointly regulate levels of neprilysin—an enzyme that breaks down amyloid-beta—in the hippocampus. In mouse models, activating the receptors raised neprilysin, reduced amyloid-beta buildup and improved memory-related behavior, the team said.
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Researchers at the University of California, Irvine report that a machine-learning system called SIGNET can infer cause-and-effect links between genes in human brain tissue, revealing extensive rewiring of gene regulation—especially in excitatory neurons—in Alzheimer’s disease.
Researchers have uncovered how amyloid beta and inflammation may both trigger synapse pruning in Alzheimer's disease through a common receptor, potentially offering new treatment avenues. The findings challenge the notion that neurons are passive in this process, showing they actively erase their own connections. Led by Stanford's Carla Shatz, the study suggests targeting this receptor could preserve memory more effectively than current amyloid-focused drugs.
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Researchers at the National University of Singapore have discovered that calcium alpha-ketoglutarate, a naturally occurring molecule, can repair key memory processes disrupted by Alzheimer's disease. The compound improves communication between brain cells and restores early memory abilities that fade first in the condition. Since it already exists in the body and declines with age, boosting it could offer a safer approach to protecting brain health.
Study links Alzheimer's origins to peripheral inflammation
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