New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
The FDA will decide whether to approve the antibody as a treatment for Alzheimer’s disease on or before March 7, 2021.
New research pushes back the age at which dementia risk from cardiovascular and metabolic factors begins. Should protective lifestyle interventions start in youth?
Homozygous carriers of GM17—a common IgG1 variant the HSV-1 virus has evolved to evade—had quadruple the risk of developing AD. In a small Swedish cohort, that is.
In updating their broad evaluation of the risk literature, the commission blamed three more modifiable factors for causing 6 percent of all dementia, concluding that 40 percent of cases can be prevented.
A slight drop in hospital admissions after amyloid PET, especially in people with positive scans, fell well short of the prespecified endpoint. Still, IDEAS is broadening into a research platform, and IDEAS 2 will add racial diversity.
New genetic variants emerged by harmonizing whole-exome-sequencing data across continents, and by using imputation to plumb the depths of existing GWAS. One variant encodes a microglial phospholipid transporter.
In the Alzheimer’s brain, too, plaques trigger a coordinated inflammatory response from microglia and astrocytes. A preprint paper had shown the same for mice.
In large population datasets, people who had been vaccinated against influenza or pneumonia appeared less likely to develop AD.
Plasma p-Tau217 Set to Transform Alzheimer’s Diagnostics Could Common Vaccines Protect Against Alzheimer’s Disease? Doubling Down on Sequencing Serves up More Alzheimer’s Genes IDEAS Finds Small Drop in Hospitalizations, Missing Goal Lancet Commission’s ...
This early marker distinguishes Alzheimer’s from controls and other neurodegenerative diseases more accurately than other biomarkers.
Poor coordination among grid cells in the entorhinal cortex and place cells in the hippocampus compromises navigation. Grid cells fail first.
This neuronal protein regulates the complement cascade in the developing brain. Could it do the same in aging or neurodegenerative disease?
In striatal spiny projection neurons with mutant huntingtin, mitochondria spill immunogenic RNAs into the cytosol. These touch off innate antiviral signaling inside the neurons, which may spell their demise.
A 2018 report that had spotted extra copies of APP lurking in neuronal genomes has come under scrutiny, with claims that the result is due to contamination. Does a response from the original authors bolster their claim?