This pathway may transmogrify microglia during neurodegeneration, without the help of TREM2.
The brain shrinkage due to verubecestat emerged quickly but did not worsen or cause neurodegeneration. Curiously, both verubecestat and lanabecestat dulled episodic memory and boosted verbal fluency.
In Barcelona, data ran the gamut from a few hopeful little hints on new treatments to mixed signals on familiar players, and failed drugs thrown on the scrap heap.
Overexpressing the endosomal activator in neurons not only caused those organelles to swell, but also bungled synaptic transmission, goaded hyperphosphorylation of tau, and destroyed cholinergic neurons.
High amyloid burden and neuroinflammation, neuronal excitability, and tangles and oligodendrocyte loss distinguish the disease types.
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.
Researchers consider the data encouraging, though questions linger about the cognition results. Did regulators mess up the randomization of this trial?
When the agency sent warning letters to 17 companies that falsely advertised cures and preventions for AD, most took down exaggerated claims. But can regulations stay ahead of the market?
Parkinson's disease is one of the most common neurodegenerative diseases, affecting about one percent of all people over the age of 65. It is characterized by rigidity, bradykinesia and tremors, which are caused by the progressive degeneration of dopamine-containing neurons...
The more risk variants in a person’s genome, the faster they decline on both cognitive and motor tests.
Topline results suggested that the anti-inflammatory treatment stabilized cognition and function over six months. The trial did not include biomarkers.
Progressive supranuclear palsy is a poorly understood movement disorder that has come to be of intense interest to age-related neurodegenerative disease researchers...
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?
In a mouse model of cortical multiple sclerosis, microglia and monocytes swooped in to gobble up synapses when dendritic calcium rose. Spines grew back once inflammation subsided.