Cdk5 Controls Memory Switch in Neurons
Research suggests that the kinase Cdk5 limits formation of new memories by keeping a key synaptic receptor away from the cell surface.
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Research suggests that the kinase Cdk5 limits formation of new memories by keeping a key synaptic receptor away from the cell surface.
Much like people with Alzheimer's, mice modelling the disease experience seizures. New research suggests that APP, and not Aβ, makes their neurons hyperexcitable.
Researchers have found protein traces of brain damage in the blood of hockey players who sustained a concussion. Could biomarkers help decide when athletes return to their sport?
A new test claims to detect Aβ oligomers in cerebrospinal fluid by exploiting their tendency to seed aggregation.
Network analysis may explain why people with semantic dementia keep making memories even as their hippocampi degenerate.
Combination therapies may work where single drugs fall short, but testing them in AD may prove challenging.
The 2014 Alzheimer’s Association report finds that women bear the brunt of AD, being more likely to develop the disease or care for someone with AD full time.
A Keystone symposium underscores the role of lysosomal dysfunction and vesicle trafficking in neurodegenerative disease.
Combination Trial Debate Energizes Keystone Symposium Protecting Neurons by Ramping Up Waste Disposal? Prodromal Initiative to Identify Biomarkers for Parkinson’s Researchers Build on GWAS to Parse Genetic Players in AD and PD More than 200 researchers br
Keystone symposium highlights new strategies in the quest to find the biomarkers of Parkinson’s disease.
Keystone presenters pulled out new tools to make connections between genetics and disease.
PINK1 mutations cripple mitochondrial energy production, raising new questions about Parkinson’s disease.
An antioxidant thought to boost mitochondrial function came up short in a large multicenter trial for PD treatment.
Astrocytes kindle neuronal hyperexcitability in mouse models of Huntington’s.
When a calcium sensor disappears from dendritic spines, synapse loss soon follows in Alzheimer’s models, aging mice, and diseased human brains.