The hippocampus trickles out new neurons throughout life, a process that falters without BACE1 or in the presence of ApoE4.
Vascular microchannels linking the skull bone marrow to the dura mater supply the brain with neutrophils in response to stroke and inflammation.
Males are inflammatory, females are neuroprotective: Profiling of microglia from adult mice suggests sex-specific phenotypes, likely set at birth.
Computational models predict that ALS mutations tax the flexibility of profilin-1, weaken binding with key partners including actin, and boost the protein’s propensity to aggregate.
By promoting the exocytosis of cellular debris, the kinase may facilitate spread of α-synuclein aggregates.
Ablating BACE1 in adult mice spares them from most problems found in germline knockouts. However, axons extending from newborn hippocampal neurons still lose their way.
Treatments that promote neurogenesis and elevate BDNF act as exercise does to improve memory in mouse models of Alzheimer’s disease.
An 856-patient, proof-of-concept trial of the anti-protofibril Aβ antibody suggests the highest dose slowed cognitive decline and cleared plaques.
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.
Reducing these esters with statins and cholesterol-hydroxylase-activating drugs lowers phospho-tau and Aβ in neurons. One such drug is approved to treat HIV AIDS.
Among cognitively normal people with amyloid plaques, women have more tau tangles in the entorhinal cortex than do men. Does this indicate susceptibility, or resilience?
In mouse models of Alzheimer’s, neutrophils stick to capillaries in the cerebral cortex, reducing blood flow. Keeping those cells moving or depleting them altogether improved memory.
A score based on the combined burden of a person’s Alzheimer’s risk variants correlated with plaques, tangles, cognitive decline, and even non-AD pathology. Are polygenic hazard scores ready for direct-to-consumer marketing?
How the element relates to neurodegeneration remains unclear.
IBM researchers in Australia identify a combination of four proteins in plasma that predicts amyloid positivity in cerebrospinal fluid, and correlates with progression to AD.