Society for Neuroscience Annual Meeting: Making the Right Mouse Model?
Several groups have reported a lack of phenotype in α-synuclein (α-S) transgenic mice, but it appears Lennart Mucke (122.10) has got it right...
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Society for Neuroscience Annual Meeting: Enzyme Mediates Aβ Degradation
Previous studies on the purification and characterization of the predominant extracellular Aβ degrading activity in the murine BV-2 microglial cell line demonstrated that insulin-degrading enzyme...
Soc for Neuroscience Ann Mtg: Novel Assay for in Vivo Catabolism of Aβ
The N- and C-terminals of synthetic Aβ1-42 were differentially labeled with 3H and 14C and then used as a probe to measure degradation by injection into rat hippocampus...
Soc for Neuroscience Annual Meeting: Novel Receptor Interaction for Aβ
That β-amyloid plays a central role in the pathogenesis of Alzheimer's disease is doubted by few investigators. However, pinning down the exact contribution amyloid makes has been remarkably difficult to accomplish...
Fibrillar Proteins in Familial British Dementia
It is likely that a process very reminiscent of that suggested for Aβ formation—fibrillar protein deposition—is to blame for the rare, inherited disorder Familial British Dementia (FBD)...
Presenting...β-Secretase
According to a report in tomorrow's Science, researchers have uncovered a strong candidate for β-secretase, the mystery enzyme that cleaves APP and allows Aβ to be formed in subsequent cleavages...
Toxic Protofibrillar Aβ
From today's Journal of Neuroscience comes evidence that intermediate Aβ species could be damaging neurons. Dean Hartley, Dennis Selkoe, and their colleagues report that so-called "protofibrillar" Aβ...
The APPsw Mouse Links ApoE to Damaged Neurons
Further evidence that apoE is needed for deposition of the fibrillar form of Aβ in plaques was presented today at the American Neurological Association's annual meeting in Seattle today...
Familial Dementia Linked to Neuroserpin Aggregation
Protein misprocessing and aggregation have been observed in many neurodegenerative diseases, including Alzheimer’s, spongiform encephalopathies, Huntington’s, Parkinson’s and FTDP-17, but it has been difficult...
Can Age-Related Memory Decline Be Reversed?
Writing in the current Nature Neuroscience, Heather Cameron and Ronald D.G. McKay report that they were able to boost the rate of neurogenesis in the hippocampus of aging rats by lowering corticosteroid levels...
APP Has a Role in Synaptic Development
In today's Journal of Neuroscience, Vivian Budnik, Laura Torroja, and their colleagues provide evidence that under normal circumstances, APP is a critical player in the formation and maintenance of synapses...
How to Misfold a Prion Protein
In the current Nature Cell Biology, Susan Lindquis and Jiang Ma of the Howard Hughes Institute at the University of Chicago report that they were able to produce abnormal prion protein (PrP) conformations from normal PrP...
Aβ and Tau Accumulation in an Animal Model of Brain Trauma
Douglas Smith and his colleagues at the University of Pennsylvania may have filled a gap in research on long-term, neurodegeneration sequelae of brain injuries...
TNF-α Reveals Another Deadly Trick
If the inflammatory cytokine tumor necrosis factor α (TNF-α) is at work in Alzheimer's disease, it may not be relying on its well-described, directly apoptotic mechanism to cause problems...
AD Mouse Model with Whole APP and PS-1 Genes
In the August issue of Nature Neuroscience, Bruce Lamb and his associates at Case Western report that they have transferred complete copies of genes for mutant human APP and PS-1 into mice that subsequently...
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