New Evidence Confirms TREM2 Binds Aβ, Drives Protective Response
The receptor responds to brain insults such as oligomeric Aβ and cellular debris by jolting microglia into clean-up mode, according to researchers at AD/PD 2017.
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The receptor responds to brain insults such as oligomeric Aβ and cellular debris by jolting microglia into clean-up mode, according to researchers at AD/PD 2017.
TIMP2 and possibly other human plasma proteins reinvigorate aged hippocampi in mice.
For their work on modifiable dementia risk factors and dementia in the oldest old, respectively, Kristine Yaffe and Claudia Kawas split this year’s coveted award in neurodegeneration research.
Need another reason to grab water instead of a soda? Beverages with added sugar—natural or artificial—are linked to smaller brain volume, worse memory, and tripled odds of stroke and dementia.
Showcasing forays into the biology of tau, researchers at AD/PD reported news on tau’s transcriptional regulation, its bungling of synaptic vesicles, its sway over the epigenome, and even flashed an atomic structure.
As the brain ages, what protects it from cognitive decline? A two-day conference focused on reserve and resilience.
Overexpressing miR-132 dampened AD pathology in young mice, and appeared to nourish the birth of new hippocampal neurons in older animals.
NIH Summit Examines What Makes a Healthy Aging Brain
Manufacturers of a therapy system called neuroAD, which combines transcranial magnetic stimulation with cognitive training, are applying for FDA marketing clearance.
Three anti-tau antibodies are in Phase 1 or 2, while an O-GlcNAcase inhibitor got the green light to start testing.
Using torpedo-like DNA snippets to delete mRNAs from cells, scientists lowered the amount of ataxin-2 protein. This allayed disease in mouse models of two neurodegenerative disorders.
Congress has opposed the Trump administration’s request to cut NIH funding, agreeing on a $2 billion boost, with a $400 million bonus for Alzheimer’s research.
People with ALS—especially those who progress fast—express myriad inflammatory genes in their blood monocytes.
Found in familial and sporadic cases of ALS, mutations in the annexin A11 gene lead to elaborate protein clumps and seem to disrupt vesicular trafficking.
A trial of an α-synuclein antibody is making use of the technology to follow subtle changes in the day-to-day function of participants.
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