Researchers identified genetic variants that may explain why some ApoE4 carriers remain free of Alzheimer’s, while some ApoE2 carriers do not.
Scientists at the AAT-AD/PD conference debuted new detection methods for this biomarker, which they say distinguished healthy controls from MCI and AD.
Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.
Besides the big-gun antibodies and BACE inhibitors, smaller, lesser-known drug programs are inching their way through the clinical trials pipeline. As is often the case, Phase 1 seems encouraging.
Despite plaques and tangles in the brain, this group, on average, maintains their cognitive skills over two to four years, suggesting the presence of resilience factors.
In response to an FDA request, the drug’s sponsor submitted new data analyses. The agency moved the action date to June 7.
In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
Mutated huntingtin may stow away in synaptic vesicles to sneak from one neuron to another.
Conformations of misfolded tau survive injection from one mouse to the next, a property shared by prions.
In mouse brain slices at least, tau shuffles in and out of protein inclusions. The tangles grew more inert as the tissue aged.
Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.
When cultured with human neurons expressing a familial Alzheimer’s gene, both microglia and astrocytes were necessary to spike complement C3 and send inflammation into overdrive.
New study finds no uptick in herpes viruses in AD. If herpes plays a role, it says, then probably it acts as an early trigger of pathology.
By comparing protein changes with GWAS data, scientists identified new links to AD. This method can unearth genes that otherwise fall short of genome-wide significance.
Among 14 familial Alzheimer’s APP mutations, two don’t change the Aβ42/Aβ40 ratio, but all of them yield long peptides of 45 to 49 residues that hide out in the membrane.