The shed domain of this microglia receptor sticks to plaques and neurons. Not so for the R47H AD variant, however.
About half of microglia in the mouse brain live as long as the whole mouse, while those in the human brain live, on average, just over four years. How does this change in Alzheimer’s?
On the heels of news that microglia mediate synaptic loss in Alzheimer’s, researchers report they may do the same in a subtype of FTD caused by progranulin deficiency.
Without the E3 ubiquitin ligase Idol, microglia readily gobble up ApoE and Aβ in a mouse model of Alzheimer’s disease.
Despite its spot on top of the pile of genetic risk factors for late onset AD, ApoE has remained an enigma on the pathophysiological level...
Independent labs report that the cholesterol transporter ABCA1 keeps brain ApoE levels high and saturated with cholesterol, but a third paper casts doubt on the link between the transporter and AD...
Everyone knows that smoking is bad for you. But there is some evidence, both epidemiological and molecular, that smokers are at reduced risk for neurodegenerative diseases such as Alzheimer's (AD) and Parkinson's (PD)...
A behavioral intervention slowed memory slippage and functional decline over two years.
Analysis of MRI brain volume data identifies multiple AD and FTD/ALS disease subtypes with distinct patterns of degeneration over time.
A small molecule that protects neurons fends off a short region of Aβ from a specific pocket on the LilrB2 receptor.
Profile matches Braak staging regions, suggesting those areas are particularly susceptible to AD pathology.
In DIAN, participants who are more physically active may also have slower disease progression.
In several model systems, α-synuclein boosts oleic acid production and the fatty acid worsens α-synuclein pathology.
In presynapses, binding sequesters synaptic vesicles.
The first rule of triage is do no harm, but try telling that to microglia...