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Ataxia in prion protein (PrP)-deficient mice is associated with upregulation of the novel PrP-like protein doppel.
The novel locus Prnd is 16 kb downstream of the mouse prion protein (PrP) gene Prnp and encodes a 179 residue PrP-like protein designated doppel (Dpl). Prnd generates major transcripts of 1.7 and 2.7Expand
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Tau Mislocalization to Dendritic Spines Mediates Synaptic Dysfunction Independently of Neurodegeneration
The microtubule-associated protein tau accumulates in Alzheimer's and other fatal dementias, which manifest when forebrain neurons die. Recent advances in understanding these disorders indicate thatExpand
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Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice
The mechanism by which mutations in the presenilin (PS) genes cause the most aggressive form of early-onset Alzheimer's disease (AD) is unknown, but fibroblasts from mutation carriers secreteExpand
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The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's Disease
Transgenic mice expressing mutant amyloid precursor proteins (APPs) have provided important new information about the pathogenesis of Alzheimer's disease (AD) histopathology. However, the molecularExpand
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The CNS glycoprotein Shadoo has PrPC-like protective properties and displays reduced levels in prion infections
The cellular prion protein, PrPC, is neuroprotective in a number of settings and in particular prevents cerebellar degeneration mediated by CNS‐expressed Doppel or internally deleted PrP (‘ΔPrP’).Expand
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Region-specific dissociation of neuronal loss and neurofibrillary pathology in a mouse model of tauopathy.
Neurofibrillary tangles form in a specific spatial and temporal pattern in Alzheimer's disease. Although tangle formation correlates with dementia and neuronal loss, it remains unknown whetherExpand
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The relationship between Abeta and memory in the Tg2576 mouse model of Alzheimer's disease.
Transgenic mice expressing mutant amyloid precursor proteins (APPs) have provided important new information about the pathogenesis of Alzheimer's disease (AD) histopathology. However, the molecularExpand
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Cerebrovascular autoregulation is profoundly impaired in mice overexpressing amyloid precursor protein.
The amyloid-beta (A beta) peptide, which is derived from the amyloid precursor protein (APP), is involved in the pathogenesis of Alzheimer's dementia and impairs endothelium-dependent vasodilation inExpand
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SOD1 rescues cerebral endothelial dysfunction in mice overexpressing amyloid precursor protein
Peptides derived from proteolytic processing of the β–amyloid precursor protein (APP), including the amyloid–β peptide, are important for the pathogenesis of Alzheimer's dementia. We found thatExpand
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Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein
Alterations in cerebrovascular regulation related to vascular oxidative stress have been implicated in the mechanisms of Alzheimer's disease (AD), but their role in the amyloid deposition andExpand
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