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.
Amyloid and tau PET are helping scientists pinpoint the underlying cause of specific AD symptoms. Perhaps imaging of certain brain regions will help predict an individual’s progression.
At the HAI 2020 conference, the tracers PI-2620 and APN-1607 appeared to bind frontotemporal dementia tau. MK-6240 looked highly sensitive. And JNJ-067 and SNFT-1 are two new kids in town.
Vision improved in some retinitis pigmentosa patients in a Phase 1 trial.
Two studies reveal new aspects of the neurovascular physiology that regulate the flow of oxygenated blood into the brain’s arterioles and capillaries in response to neuronal stimulation.
The protease suppresses Aβ in Down’s syndrome organoids.
Post-translational modifications differ from those in AD tau fibrils, and may dictate tau strains.
The creation of long-term memories requires a continual supply of myelin provided by newly formed oligodendrocytes. Alas, the generation of fresh oligodendrocytes diminishes with age, along with memory.
FDA approves adding safety and efficacy data from an Alzheimer’s trial to the drug’s label.
DIAN, Roche, Lilly disclose that neither gantenerumab nor solanezumab slowed cognitive decline in the first-pass comparison of drug and placebo groups. Analyses are ongoing; dose may have been too low.
Synapse loss and mitochondrial stress, as seen by separate PET tracers, go hand-in-hand in Alzheimer’s, Parkinson’s, and frontotemporal dementia.
New research presented at the HAI conference also finds links between UCB-J uptake and plaques, tangles, and cognitive decline.
PET Tracer Detects Synapse Loss Across Alzheimer’s Brain Multimodal Imaging of Neurodegenerative Diseases Links Pathology and Cellular Dysfunction Tau PET: The Field Expands Rapidly Can PET Match Up Areas of Protein Deposit With Alzheimer’s Symptoms? As ...
Quite independently of what it does to Aβ or tau, ApoE4 stokes α-synuclein pathology in mouse models. People with Lewy body dementia who carry ApoE4 had more phosphorylated synuclein in their brains, and their cognition declined faster.
Researchers implicate PrP in the toxicity of Aβ, tau, and α-synuclein oligomers in several neurodegenerative diseases.
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