Could Adaptive Immunity Set the Brakes on Amyloid?
Genetic and animal studies hint that B and T cells control amyloid accumulation, though the mechanisms remain unclear.
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Genetic and animal studies hint that B and T cells control amyloid accumulation, though the mechanisms remain unclear.
The growth factor turns off microglia, major support cells for neurons.
At AD/PD, researchers further tied TREM2 to phagocytosis and enumerated markers that may distinguish beneficial microglia from harmful ones.
A new study suggests that tau oligomers as small as trimers enter neurons and corrupt native tau proteins inside.
In a Solomonic move, a prestigious prize for research in neurodegenerative disease goes to a veteran tauist and a self-professed inhabitant of “amyloid land.”
A protein instigates axon degeneration by promoting destruction of the essential enzyme cofactor, NAD+.
A NexGen prevention trial in familial Alzheimer’s mutation carriers will shoot for flexible testing of high doses and drug combinations.
Researchers identify N-terminally extended Aβ peptides that are toxic to synapses and rise after BACE1 inhibition, though whether they occur in human disease remains unclear.
Researchers report the highest resolution structure to date for γ-secretase, the multisubunit complex that churns out Aβ.
The approach plays neuroinflammation against neurodegeneration. It may be too risky for people because it would instigate multiple sclerosis, but yields information on the choroid plexus.
People with at least 16 years of education are less likely to accumulate markers of neurodegeneration in their brains, says a cross-sectional study.
Several different striatal markers may help researchers track early deterioration in Huntington's and Parkinson’s diseases.
Knockout mice lived to old age with mild brain abnormalities but no sign of motor neuron disease.
A discontinued β-secretase blocker reportedly quieted inflammation and cleared amyloid plaques by way of microglial activation.
A stem cell model suggests the β-secretase-generated C-terminal fragment of the amyloid precursor protein raises tau protein levels.
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