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Less than two weeks after announcing that memantine had shown significant benefit in a clinical trial of patients with moderate to severe Alzheimer's disease, Forest Laboratories announced that they have withdrawn their New Drug Application with the FDA...
Forest Laboratories, Inc., reported last week that patients with moderate to severe Alzheimer's disease taking memantine and donepezil had significant improvement over patients on donepezil alone on tests of cognitive and daily functioning...
The European Union's Committee of Proprietary Medicinal Products (CPMP) has recently recommended that the EU approve <a href="/therapeutics">memantine</a> for the treatment of moderately severe to severe Alzheimer's disease...
On May 29 and 30, the New York City-based <a href="http://www.aging-institute.org/venture.htm">Institute for the Study of Aging</a> convened a small symposium to take the pulse of current research on ApoE, the leading risk factor for nonfamilial AD...
I-han Chou reports from Brain Mapping Conference in New York City.
In a sparsely attended slide presentation yesterday at the Neuroscience meeting, <strong>Inez Vincent</strong> of the University of Washington, Seattle, presented a feat no one seems to have pulled off before...
The more scientists learn about γ-secretase, the crazier it looks to them...
In last Friday's Nature, Lawrence Goldstein of the University of California, San Diego, further advanced his claim that the amyloid-β precursor protein (AβPP) mediates fast, anterograde axonal transport by binding to the motor protein kinesin-1...
Read Peter Davies’ summary of this meeting, organized by Eva-Maria Mandelkow and Ulrike Beisiegel.
Polyglutamine (poly Q) expansion in the huntingtin protein (htt) causes Huntington's disease (HD), yet it remains unclear clear how this expansion induces the cellular and neurological damage of the disease...
A new mouse model of a CAG repeat disorder supports the hypothesis that soluble mutant proteins might be more dangerous than aggregates in some neurodegenerative diseases...
It is well known that an expanded polyglutamine tract (polyQ) within the huntingtin (htt) protein is the root cause of Huntington's disease (HD), but just exactly how this polyQ expansion exerts its devastating effects...
Two papers in the 25 September Neuron move axonal transport squarely into the limelight of research on triplet-repeat (or polyQ) diseases, including Huntington’s...
An advanced online publication in today’s Nature Neuroscience lends support to the hypothesis that mitochondrial damage contributes to the progression of Huntington’s disease...
In this week’s Neuron, researchers report that polyglutamine-expanded huntingtin (Htt)—the direct cause of Huntington's disease—exacerbates inositol triphosphate-mediated calcium signaling...
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