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.
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.
The microbial communities teeming in the intestine of people recently diagnosed with PD differed markedly from those of healthy controls.
Three anti-tau antibodies are in Phase 1 or 2, while an O-GlcNAcase inhibitor got the green light to start testing.
Manufacturers of a therapy system called neuroAD, which combines transcranial magnetic stimulation with cognitive training, are applying for FDA marketing clearance.
NIH Summit Examines What Makes a Healthy Aging Brain ...
Overexpressing miR-132 dampened AD pathology in young mice, and appeared to nourish the birth of new hippocampal neurons in older animals.
As the brain ages, what protects it from cognitive decline? A two-day conference focused on reserve and resilience.
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.
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.
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.
Tau antibodies in the blood bind and stabilize tau as it leaves the brain, offering researchers a readout of soluble tau levels in the CNS.
TIMP2 and possibly other human plasma proteins reinvigorate aged hippocampi in mice.
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.
In tauopathy mice, ApoE4 hastened neuroinflammation and neurodegeneration. No amyloid involved. (Tip: Think A1 astrocytes.)
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