How Much Amyloid Will Kick Off Tangles, and Decline?
At HAI 2020, scientists more precisely quantified the relationship between plaques, tangles, and cognitive decline.
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At HAI 2020, scientists more precisely quantified the relationship between plaques, tangles, and cognitive decline.
By engaging scientists studying every tau-based disorder, a new conference aimed to foster collaborations and research directions.
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?
At the at Tau2020 conference, scientists show high-resolution cryoEM of α-synuclein. Two different types of fibril are composed of asymmetric protofibril units.
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.
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.
At Tau2020 conference, scientists implicate LDL receptor-related protein 1 in cell-to-cell transmission.
The monoclonal antibody activated TREM2 signaling on mouse microglia. It supported their survival and stimulated their clearance of amyloid plaques.
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.
A survey conducted by the Alzheimer’s Association finds that three-quarters of these physicians had little to no residency training in dementia care.
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 the human brain, alpha waves fell out of sync, while delta-theta waves swelled in concert with amyloid plaques, neurofibrillary tangles. Alpha modulation correlated with cognitive decline.
In a conditional mouse knockout, lack of neuronal BIN1 slowed excitatory signaling, leading to spatial memory problems. Could this play a role in Alzheimer’s?
The slowdown of proteasomes stymied TDP-43’s entry into the nucleus and promoted its aggregation in the cytoplasm.
Under diabetic conditions, SERP1 binds secretase subunit, cranking up cleavage of APP but not Notch. The finding offers a mechanistic link between diabetes and Alzheimer’s.
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