The modified protein prevents the synaptic protein KIBRA from managing plasticity.
Not exosome, not proteasome, not autophagy: Could a new pathway dubbed MAPS facilitate the spread of amyloidogenic proteins?
Claims of a positive effect in a small subgroup of patients are statistically meaningless, experts say.
The monoclonal antibody appears to remove plaques, although the small trial could not draw conclusions about cognition.
The LAG3 transmembrane protein latches onto fibrillar forms of the synaptic protein and ushers them into neurons. Researchers propose targeting LAG3 to slow toxic spread of misfolded forms of synuclein.
Despite conflicting results in the past, a large new study analyzing multiple statins in different ethnic groups suggests a protective effect from this class of medication.
Restoring normal transport of BACE1-carrying endosomes prevents synapse loss and cognitive decline in mice.
In a bizarre twist of cell biology, researchers find proteasomes in the neuronal plasma membrane. They pump signaling peptides into the extracellular space.
A new fluorescent compound labels only non-contractile cells in the capillary bed, supporting the idea that these mysterious little cells do not directly regulate brain blood flow.
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.