Spewed by stressed microglia, fragments of the organelles provoke mitochondrial fission in other cells, causing astrogliosis and neuronal loss.
In neurons derived from FTD patients, morphological changes at the base of the axon render them hyperexcitable.
In animal models and patient-derived neurons, terazosin elevated ATP and warded off neurodegeneration. Men who take the drug to control prostate hyperplasia are less likely to get PD, or have milder symptoms.
The study halted early when the primary endpoint was met, but an unusual trial design and lack of detailed data leave questions unanswered.
A chemist at the University of Cambridge, Dobson developed equations that described the kinetics of protein aggregation in diseases such as Alzheimer’s.
In induced human microglia, the E4 allele profoundly affected their health and cellular responses, while familial Alzheimer’s mutations had little effect.
Biogen and Eisai announced the discontinuation of the Phase 3 program. Elenbecestat was the only remaining BACE inhibitor being tested for AD.
The Phase 2 study missed its primary endpoint. While fewer developed dementia in the treatment group, the effect was not statistically significant. People on drug had less brain atrophy than those on placebo.
New data strengthen the idea that a healthy locus coeruleus keeps memory sharp into old age.
The organelles express unique sets of proteins depending on their environment. Astrocyte mitochondria process lipids better than those in neurons.
The pattern varied from person to person, depending on the site of injury, in contrast to the stereotyped distribution of tau tangles seen in Alzheimer’s disease.
In patient-derived neurons, tau mutations scupper lysosomes and SORLA shunts APP through different types of endosomes.
The protein forms cohesive rafts along microtubules, protecting them from digestion and regulating movement of molecular motors.
Eliminating microglia in a mouse model of amyloidosis nearly abolished parenchymal plaques, but led to a huge buildup of amyloid in cerebral blood vessels.
Passive monitoring of old people in their everyday lives is starting to generate new indicators for cognitive impairment.