This new inhibitor, which only works once phosphorylated by GSK3, reduced amyloid load and prevented cognitive deficits in an AD mouse model.
At least one phosphate tag may quell Aβ excitotoxicity.
The wireless implant converts signals from the patient’s motor cortex into type. This is the first such device to be used in a home setting.
Drawing on longitudinal ADNI data, a new study suggests that the degeneration of cholinergic neurons in the basal forebrain kicks off the neurodegenerative cascade of AD.
Fluselenamyl avoids white matter and binds diffuse plaques
Two international initiatives compile metadata from aging and AD studies into huge searchable catalogs in hopes of speeding research progress.
Before any other changes, the fatty coating on peripheral nerve fibers breaks apart, heralding their degeneration.
Trial sponsors moved children from ongoing trials to open-label studies following positive interim results of an antisense oligonucleotide treatment.
A synthetic amyloid harmed cultured cells only when it deprived them of an essential protein.
Mice expressing a mutant version of human UBQLN2 develop TDP-43 pathology in their spinal cords, while losing motor neurons, muscle mass, and muscle innervation of with age.
As reported at meetings, Merck’s BACE inhibitor reduced CSF Aβ in animals and people with apparently few side effects. Researchers express optimism for the drug and others in its class.
In Italian memory clinics, the PET scans resulted in diagnosis and medication changes for up to a third of patients.
In development, the brain follows a set of rules when it folds to form its ridges and grooves. Those rules change with age, and especially in Alzheimer’s.
Despite no warning signs in ongoing clinical trials, researchers are searching for safer drugs, and better biomarkers to measure what they do.
In Seeon, researchers reported that blocking the protease may heal dystrophic neurites and repair electrical activity.