Researchers may soon add another imaging agent to their tool kit—one that tracks synapse loss.
At Keystone, researchers also linked the receptor to microglial homeostasis and migration, and resolved lingering questions about TREM2’s role in plaque clearance.
A PET study comparing amyloid, tau, and volumetric imaging in preclinical AD identifies a region where local tangles correlate with brain-wide amyloid.
People who report a prior head injury have no more chance of getting Alzheimer’s than the rest of the population, but they may be at higher risk for Parkinson’s.
Researchers are discovering that microglia not only respond dramatically to their environment, but they also can quickly lose their identity.
At Keystone, researchers report the discovery of ion channels that shed light on the machinations of the brain’s microglia.
A bill approved by the U.S. House Committee on Appropriations would increase funding for Alzheimer’s by $350 million.
Could similar immune dysfunction contribute to neurodegeneration in people who carry repeat expansions in one copy of the gene?
Did you know Alzforum first launched exactly 20 years ago, in July 1996, at the International Conference on Alzheimer Disease in Osaka, Japan? We will mark this milestone in our mission to advance the field of Alzheimer’s and neurodegenerative disease research at the upcoming Alzheimer’s Association International Conference in Toronto. Wish us happy birthday by swinging by the Alzforum booth, #724. Meet our team, take a tour of AlzBiomarker and Alzforum’s many other resources, and snag an anniversary gift we made to celebrate progress in AD research.
Plaques, tangles, and now synapses? A new PET ligand on the horizon binds a protein found in synaptic vesicles. With all the makings of a solid PET tracer, the compound appears to track synaptic density in monkeys and in people, and easily detects synapse loss in patients with epilepsy. It now stands poised for its debut in Alzheimer’s disease and other disorders that tear down connections between neurons.
With PET, researchers can now image the neurofibrillary tangles and amyloid plaques of Alzheimer’s disease in the living brain. In cognitively healthy elderly, the two pathologies occur independently for the most part, but they do correlate with each other in certain key brain regions, according to a new study. In particular, pathological tau in the inferior lateral temporal cortex tracked with the presence of widespread plaques. The findings may provide clues to what kicks off the earliest stages of disease.
Microglia constantly survey the brain. They listen to a cacophony of signals from neurons and other cells, and sample molecules floating in the parenchyma. How do they do it? From super-enhancers that make these cells unique, to transcriptomes that characterize their response to neurodegeneration, to ion channels that power their motility, scientists are learning more about these immune cells of the brain. Read the latest two stories from the recent Keystone symposium.
A new data-driven model of dementia progression claims that disruptions to the brain vasculature precede amyloid plaques, neurofibrillary tangles, neurodegeneration, and cognitive decline in ADNI cohorts. The findings rely on an abnormality index calculated for each marker. They are at odds with prior cross-sectional and longitudinal studies that place Aβ markers first in Alzheimer’s disease. Does the model favor the vascular hypothesis of AD, or might other factors explain this order, such as heterogeneity among study volunteers? Read the numerous comments evoked by Jessica Shugart’s story on the paper.
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- Roberto Malinow on Next Up for Human Brain Imaging: Synaptic Density?
- Stephen Salloway on Next Up for Human Brain Imaging: Synaptic Density?
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