Alzheimer

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.

09. maaliskuuta 2026 Raportoinut AI Faktatarkistettu

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 the University of California, San Francisco, have discovered a mechanism by which exercise helps protect the brain from age-related damage associated with Alzheimer's disease. Physical activity prompts the liver to release an enzyme that repairs the blood-brain barrier, reducing inflammation and improving memory in older mice. The findings, published in the journal Cell, highlight a body-to-brain pathway that could lead to new therapies.

17. helmikuuta 2026 Raportoinut AI Faktatarkistettu

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.

University of Michigan researchers using fruit flies report that changes in sugar metabolism can influence whether injured neurons and their axons deteriorate or persist. The work, published in *Molecular Metabolism*, describes a context-dependent response involving the proteins DLK and SARM1 that can briefly slow axon degeneration after injury, a finding the team says could inform future strategies for neurodegenerative disease research.

26. tammikuuta 2026 Raportoinut AI

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.