Primary Care Physicians Unprepared to Handle Future Alzheimer’s Case Loads
A survey conducted by the Alzheimer’s Association finds that three-quarters of these physicians had little to no residency training in dementia care.
A survey conducted by the Alzheimer’s Association finds that three-quarters of these physicians had little to no residency training in dementia care.
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.
The monoclonal antibody activated TREM2 signaling on mouse microglia. It supported their survival and stimulated their clearance of amyloid plaques.
At Tau2020 conference, scientists implicate LDL receptor-related protein 1 in cell-to-cell transmission.
Autopsy data confirm that current tau PET tracers are unsuitable for some primary tauopathies. CryoEM structures help researchers find new ligands for tau and α-synuclein.
Not sure where that is? You are not alone. It is a tiny spot deep behind the nose, newly defined by the PET signal of early neurofibrillary tangle deposition. It also prompted a tau-staging scheme.
At the at Tau2020 conference, scientists show high-resolution cryo-EM of α-synuclein. Two different types of fibril are composed of asymmetric protofibril units.
Centenarians who scored high on the MMSE stayed cognitively and physically active over the next two years, even if they carried genetic risk factors for Alzheimer’s. What protects these lucky few?
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome F. Hoffmann-La Roche, joining our other exhibitors — Biogen, BioLegend, Dash Genomics, Inc., Abcam, BrainXell, and the Jackson Laboratory.
TREM2 signaling supports all manner of microglial functions, and a new monoclonal antibody dials this diehard support up a notch, at least in mice. Dubbed 4D9, the antibody latches onto the extracellular region of TREM2, preventing its release from the cell surface by hungry proteases. The resulting intracellular signaling bolstered microglial survival and rousted the cells into mopping up Aβ in the brain. A human version of the antibody is moving toward clinical trials.
Sponsored by the Alzheimer’s Association, CurePSP, and the Rainwater Charitable Foundation, Tau2020 convened scientists who don’t often cross paths. The 650 attendees included researchers who study primary tauopathies, including frontotemporal dementia, and those who focus on secondary tau diseases, such as Alzheimer’s. The organizers hoped that the meeting would foster new ideas and collaborations. Over two days, all aspects of tau biology were dissected, from genetics, to proteostasis, to PET imaging. Read Tom Fagan’s highlights.
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