Caspase-2 May Unleash Soluble Toxic Tau Fragment
The fragment crowds into synapses and may drag full-length tau along for the ride. Researchers proposed caspase-2 as a therapeutic target.
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The fragment crowds into synapses and may drag full-length tau along for the ride. Researchers proposed caspase-2 as a therapeutic target.
Preserved brain networks may explain the exceptional memory prowess of some older adults.
The mysterious protein made by the ALS/FTD-associated gene may regulate the actin filaments that physically support axons.
Researchers at the Kloster Seeon meeting pressed in on the question of what are the physiological functions of this protease after development is complete.
At 2nd Kloster Seeon Meeting, Renewed Optimism for Targeting BACE1 What Exactly Does BACE Do in Adults? BACE Inhibition and the Synapse—Insights from Seeon Does BACE Drive Neurites into Dystrophy, Shorting Circuits? Will Next-Gen BACE Inhibitors Dodge Sid
At the 2nd Kloster Seeon meeting on BACE proteases, researchers linked BACE substrates to regulation of synaptic activity.
In Seeon, researchers reported that blocking the protease may heal dystrophic neurites and repair electrical activity.
Despite no warning signs in ongoing clinical trials, researchers are searching for safer drugs, and better biomarkers to measure what they do.
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.
In Italian memory clinics, the PET scans resulted in diagnosis and medication changes for up to a third of patients.
Two international initiatives compile metadata from aging and AD studies into huge searchable catalogs in hopes of speeding research progress.
Trial sponsors moved children from ongoing trials to open-label studies following positive interim results of an antisense oligonucleotide treatment.
Before any other changes, the fatty coating on peripheral nerve fibers breaks apart, heralding their degeneration.
Fluselenamyl avoids white matter and binds diffuse plaques
Insulin delivered directly to the brain does nothing to Aβ in an AD mouse model, complicating the relationship between diabetes and Alzheimer’s.