The blood-based marker may be far more scalable and cost-effective for tracking the disease than PET imaging and CSF biomarkers.
Among people with early AD, the monoclonal antibody wiped out Aβ plaques and slowed cognitive and functional decline by a third, relative to placebo.
Topline results suggested that the anti-inflammatory treatment stabilized cognition and function over six months. The trial did not include biomarkers.
Aging macrophages and microglia poorly burn glucose and enter an inflammatory state. Revving their metabolism preserved synapses and memory in mice. What does prostaglandin have to do with it?
Some people with severe COVID-19 have neurovascular injury and elevated markers of neural damage in their blood and CSF. What’s going on in their brains?
Plaque-ridden 5xFAD mice were no better at fending off an intracerebral herpes virus infection than their wild-type counterparts. The virus was not to be found within Aβ plaques and did not spur plaques to form.
Researchers identified genetic variants that may explain why some ApoE4 carriers remain free of Alzheimer’s, while some ApoE2 carriers do not.
Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.
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 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.
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.