345629 RESULTS
RESEARCH NEWS 2000-07-03 Research News Finding a safe way to get therapeutic genes past the blood-brain barrier has led to some interesting approaches using the barrier's own transport systems to shuttle DNA across the blood capillary wall from the bloodstream into the brain
RESEARCH NEWS 2000-07-03 Research News 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 release amyloid-β. In fact, say these authors, the results l
RESEARCH NEWS 2000-06-30 Research News 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 treatment
RESEARCH NEWS 2000-06-26 Research News 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, perhaps by regulating circadian
CONFERENCE COVERAGE 2000-06-17 Conference Coverage Peter Lansbury, like I and others, has long promulgated the idea that intermediates in CNS disease-related fibrillogenesis processes are likely to be pathogenic, whereas mature matted fibrils (although not desirable) are relatively ine
CONFERENCE COVERAGE 2000-06-17 Conference Coverage Last July, Dale Schenk and colleagues from Elan Pharmaceuticals reported the remarkable observation that simple immunization of PDAPP transgenic mice with amyloid-forming peptide sequences both prevents plaque formation and ameliorates
RESEARCH NEWS 2000-06-14 Research News Creatine, increasingly popular as a dietary and exercise supplement, has shown the ability to counteract laboratory models of amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease), Huntington's disease, and Parkinson's
RESEARCH NEWS 2000-06-08 Research News The true identity of γ-secretase, the enzyme that frees amyloid-β from its membrane-bound precursor, is one of the holy grails in the search for the cause of Alzheimer's disease. A battery of circumstantial evidence has recently focused
RESEARCH NEWS 2000-05-19 Research News 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 that trigger this reaction, report Li-Huei Tsai
RESEARCH NEWS 2000-05-19 Research News According to a report in today's Science, a productive approach to combating the spongiform encephalopathies such as the transmissible "variant" Creutzfeldt-Jacob disease (vCJD, popularly known as "mad cow disease")
COMMENT Reply to Sam Gandy by Gunnar Gouras We all agree that "full-blown" structural pathology (plaques and tangles) precede and accompany dementia. What we are especially considering is whether there is any role for intraneuronal Aβ in causing neurona
WEBINAR 2000-05-16 Gunnar Gouras led this live discussion on 16 May 2000. Readers are invited to submit additional comments by using our Comments form at the bottom of the page. Transcript: Live discussion held 16 May 2000. Participants: Bruce Yankner, Huaxi Xu, Austin Ya
COMMENT From various studies examining the toxicity of Aβ, it is clear that random coil monomeric Aβ is not toxic whereas oligomeric aggregates (protofibrils, ADDLs or fibrils) are. Thus the critical issue with respect to Aβ toxicity is its aggregation state. An
COMMENT The idea that intracellular Aβ injures neurons and causes dementia prior to the formation of extracellular deposits is not obviously reconcilable with other evidence indicating that "full-blown" structural pathology precedes dementia (Crystal H,
RESEARCH NEWS 2000-05-08 Research News The DNA sequence of human chromosome 21 will be published electronically today in Nature (and in print on 18 May). This achievement, by an international consortium of 62 scientists in Japan, Germany, France, Switzerland, the USA and Britain,
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