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Toward Visualizing Plaques in Vivo

One of the challenges to diagnosing Alzheimer's disease is the lack of a nonbehavioral clinical test. The definitive diagnosis can only be made when amyloid plaques and neurofibrillary tangles are seen at autopsy...

Noose Tightens Around Presenilin

Results presented by three research groups this week all confirm that presenilin is, at the least, essential for γ-secretase to cleave amyloid precursor protein in the process that releases amyloid-β-...

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...

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