The Mutation You Want: It Protects the Brain, Extends Life
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
78 RESULTS
Sort By:
A PLCG2 variant that reduces a person’s risk of Alzheimer’s, frontotemporal dementia, and dementia with Lewy bodies also appears to extend longevity.
Serial amyloid and tau scans in cognitively healthy people indicate that the speed at which a person’s tau accumulates best predicts his or her future cognitive decline.
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.
Perturbations in the hormone correlate with memory problems. But does FGF23 act in the brain, or affect cognition indirectly via the kidneys?
Atomic resolution structures of tau filaments from three people with CTE revealed a common strain of tau induced by chronic head injuries.
Using rigorous tissue-processing techniques, researchers find thousands of newborn neurons in older human hippocampi, but a dearth in brains with AD pathology.
Blocking the receptor clears toxic proteins and improves memory in old mice. The work proposes a new role in microglia for a well-known B-cell receptor.
Microglia cleanup, mitophagy, axonal plasticity, blood-brain barrier. A renewed focus on ApoE4 is revealing new ways in which this isoform renders the brain vulnerable to Alzheimer’s.
In a research study, one-fifth of healthy people who learned they were at high risk for AD said they might consider physician-assisted death as a future option.
“We are learning” was the tenor of debate about the latest round of setbacks for anti-amyloid trials in symptomatic Alzheimer’s disease at a recent conference in Lisbon.
Chemotherapy riles microglia, causing neurons to turn down expression of BDNF, a growth factor necessary for myelination. Restoring BDNF signaling on oligodendrocytes spared myelin and memory loss.
A prospective progeria drug revs up cellular autophagy and clears tau in neurons derived from patients with frontotemporal dementia. In mouse models, the drug rescues abnormal behavior.
Senolytic drugs kill these cells, temper Aβ, and improve cognition in transgenic mice.
The method purportedly distinguishes patients from controls with more than 90 percent sensitivity and specificity.
In people carrying two mutated copies of the trophic receptor, important brain structures, such as the corpus callosum, never developed.