As gene therapy is making a comeback, scientists are exploring if it might prevent or reverse Alzheimer’s. Some of those treatments are permanent, heightening safety concerns.
Three studies found no link between vascular disease and cerebral amyloidosis.
Happy New Year, readers! Yes, 2019 has passed, but so much happened last year that capturing the essence took longer than usual. Our mega year-end story is now posted for your reading pleasure.
Two epigenetic proteins accelerated age-related behavioral decline in worms and in mice, at least partly by dampening mitochondrial function. Orthologs in the human brain ramped up with aging and with AD progression.
In motor neurons of TMEM106b knockout mice, swollen vacuoles piled up in axons near the soma, rendering the mice wobbly and slow to react. The finding contradicts prior reports.
Different forms of p-tau in cerebrospinal fluid reflect worsening plaque load, metabolism, and atrophy in the brain. They could help stage Alzheimer’s disease.
In people with Alzheimer’s biomarkers, the basal forebrain shrinks early, foreshadowing microglial neurotoxicity, atrophy in the medial temporal lobe, and cognitive decline.
For people with Parkinson’s, carrying Alzheimer’s genetic risk variants upped their odds of harboring Aβ and tau pathology and getting dementia. In people with DLB, Aβ plaques worsened tau and Lewy pathology, and cognition.
Avid’s postmortem validation data indicate Alzheimer’s can be diagnosed by visual examination of flortaucipir PET scans.
Award recognizes discoveries of genetic variants that perturb liquid-liquid phase separation and increase risk for ALS-FTD and other neurodegenerative diseases.
Umbilical cord stem cells from presenilin 1 E280A carriers, once differentiated into cholinergic-like neurons, pumped out Aβ42 and accumulated phosphorylated tau and apoptotic markers.
Induced neurons lacking the Alzheimer’s risk gene can’t properly recycle APP.
In stark contrast to Aβ and tau fibrils, α-synuclein fibrils are asymmetric, comprising two different protofibrils.
In cell culture, slashing Aβ production by more than half harmed neuronal signaling, but a smaller cut maintained it.
A half-dozen lesser-known compounds in trials for Alzheimer’s disease posted results at the CTAD conference.