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Huntington's Damages May Be Reversible

The discovery that Huntington's disease results from a particular mutation of the gene for the protein dubbed "huntingtin" has created great hope that this neurodegenerative movement disorder will soon have effective treatments...

Finding the Time to Store a Memory

How are short-term memories converted to long-term memories? The process is certain to be complex, and a study in the 23 June issue of Science suggests thetranscription factor NPAS2 may play an important role...

The Calpain Connection

The cysteine protease calpain cleaves the cdk5 regulator p35, releasing a 25KD fragment that accumulates in the brains of people with Alzheimer’s disease. What’s more, Aβ42 is among the factors...

Slowing the Scrapie Prion

According to a report in today's Science, a productive approach to combating the spongiform encephalopathies such as the transmissible "variant" Creutzfeldt-Jacob disease may be to attack cells in the spleen where...

Do Aβ and APP Team up to Kill Neurons?

Many researchers believe that the amyloid-β peptide is a culprit in the neurodegenerative process of Alzheimer's disease. Indeed, they can marshal good evidence that the fibrillar form of Aβ kills neurons in a petri dish...

Another Fatal Peptide from APP

Some of the attention focused on amyloid-β may have to be diverted to yet another peptide product of amyloid precursor protein (APP). Daniel Lu, Edward Koo and colleagues report in the April issue of Nature Medicine that...

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