Researchers implicate these innate immune cells in the disruption of neurovascular coupling by Aβ in mice.
White blood cells from certain Parkinson’s patients react to α-synuclein peptides. Is this autoimmune reaction why the major histocompatibility complex is genetically linked to the disease?
Gaps surrounding blood vessels in the brain may predict cognitive decline and vascular dementia.
The aging brain winds down rapid glucose metabolism in regions that will go on to accumulate amyloid, perhaps raising the risk of neurodegeneration.
Researchers debut a statistical model that uses MRI, CSF, and demographic data to compute a cognitively impaired person’s risk for progressing to dementia.
Mutations spur fibrillization, while methylation and autophagy keep droplets nice and fluid.
A new study provides the first solid evidence for a loss-of-function mechanism in ALS caused by C9ORF72 repeat expansions.
People with inflammatory bowel disease are at higher risk for Parkinson’s—but not if they take anti-inflammatory medication.
Contrary to previous findings, both proteins seem to escape via passive diffusion. This has implications for therapeutic strategies to keep them where they belong.
The 2019 budget ups this year’s spending by $425 million.
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...