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The existence of a phonemic deficit that is predictive of, and probably causal to, many cases of reading difficulty is well established. Tallal (1984) has suggested that this phonemic deficit is in fact a symptom of an underlying auditory temporal processing deficit. Our purpose in this paper is to evaluate the plausibility of this hypothesis. The various(More)
It has recently been claimed (Geiger & Lettvin, 1987; Perry, Dember, Warm, & Sacks, 1989) that the acuity/eccentricity function is flatter in dyslexics than in normal subjects, with dyslexics showing better performance in the periphery and worse performance at fixation. In these studies, all target letters were presented to the right of fixation, a(More)
BACKGROUND Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disorder originating from exposure to bovine-spongiform-encephalopathy-like prions. Prion infections are associated with long and clinically silent incubations. The number of asymptomatic individuals with vCJD prion infection is unknown, posing risk to others via blood(More)
Alzheimer's disease (AD) is associated with pathological assembly states of amyloid-β protein (Aβ). Aβ-related synaptotoxicity can be blocked by anti-prion protein (PrP) antibodies, potentially allowing therapeutic targeting of this aspect of AD neuropathogenesis. Here, we show that intravascular administration of a high-affinity humanized anti-PrP antibody(More)
Currently, no treatment can prevent the cognitive and motor decline associated with widespread neurodegeneration in prion disease. However, we previously showed that targeting endogenous neuronal prion protein (PrP(C)) (the precursor of its disease-associated isoform, PrP(Sc)) in mice with early prion infection reversed spongiform change and prevented(More)
Prion diseases are fatal neurodegenerative conditions for which there is no effective treatment. Prion propagation involves the conversion of cellular prion protein, PrP(C), to its conformational isomer, PrP(Sc), which accumulates in disease. Here, we show effective therapeutic knockdown of PrP(C) expression using RNAi in mice with established prion(More)
Mutations in the charged multivesicular body protein 2B (CHMP2B) gene cause frontotemporal lobar degeneration. The mutations lead to C-terminal truncation of the CHMP2B protein. We generated Chmp2b knockout mice and transgenic mice expressing either wild-type or C-terminally truncated mutant CHMP2B. The transgenic CHMP2B mutant mice have decreased survival(More)
A number of points and criticisms were raised in the commentaries on our review paper (Farmer & Klein, 1995), and in this reply we address the most pertinent and major of those points. First, we clarify and expand upon what we mean by a temporal processing deficit. We then address Studdert-Kennedy and Mody's (1995) major claims, which are confined to the(More)
In the post-genomic era, the laboratory mouse will excel as a premier mammalian system to study normal and disordered biological processes, in part because of low cost, but largely because of the rich opportunities that exist for exploiting genetic tools and technologies in the mouse to systematically determine mammalian gene function. Many robust models of(More)