Risk alleles of SORL1 dampen its expression in response to growth factors, leading to higher Aβ production.
When ultrasound opens the blood-brain barrier in mice, microglia engulf plaques.
A risk allele previously linked to Parkinson’s is now extended to Alzheimer’s as well, with particularly strong effects in patients who lack an ApoE4 allele.
In mice lacking BACE1, fewer potassium ions escape hippocampal neurons, causing brain cells to fire more rapidly.
Mice expressing presenilin harboring AD-associated mutations resemble mice lacking the enzyme altogether, suggesting that the mutations fully inactivate the enzyme.
The brain’s resident immune cells secrete galectin-3, which activates other nearby microglia to promote neuroinflammation.
Simple survey touted as a potential functional outcome in prevention trials.
In mice, the presence of mutant human tau disrupts synaptic signaling and slows down neuronal firing.
The Journal of Neuroscience retracted a paper that claimed Aβ does not accumulate inside neurons, and temporarily banished its senior authors.
Researchers at a Keystone meeting proposed that quelling inflammation outside the brain could slow the progression of Alzheimer’s and other neurodegenerative diseases.
Whether cleaning up plaques in AD or mopping up debris in the wake of a stroke, microglia get by with a little help from TREM2.
Large consortium releases epigenome profiles of 111 different tissues. They are already yielding insight into the immune system’s role in Alzheimer’s disease.
Skin side effect under investigation.
Routine cognitive screening could help doctors spot people at risk of dementia. Two new tests could make screening more accessible.
A debate has sprung up in response to a Cell essay arguing that the baby was thrown out with the bathwater when a γ-secretase inhibitor failed in Phase 3.