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Kenneth L. Davis

Researcher at Icahn School of Medicine at Mount Sinai

Publications -  625
Citations -  65560

Kenneth L. Davis is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Schizophrenia & Alzheimer's disease. The author has an hindex of 113, co-authored 622 publications receiving 61120 citations. Previous affiliations of Kenneth L. Davis include University of North Carolina at Charlotte & Case Western Reserve University.

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Biological insights from 108 schizophrenia-associated genetic loci

Stephan Ripke, +354 more
- 24 Jul 2014 - 
TL;DR: Associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses.
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A new rating scale for Alzheimer's disease.

TL;DR: A new rating instrument, the Alzheimer's Disease Assessment Scale, was designed specifically to evaluate the severity of cognitive and noncognitive behavioral dysfunctions characteristic of persons with Alzheimer's disease.
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Dopamine in Schizophrenia: A Review and Reconceptualization

TL;DR: The authors hypothesize that schizophrenia is characterized by abnormally low prefrontal dopamine activity leading to excessive dopamine activity in mesolimbic dopamine neurons (causing positive symptoms) and has important implications for treatment of schizophrenia and schizophrenia spectrum disorders.
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Mapping autism risk loci using genetic linkage and chromosomal rearrangements

Peter Szatmari, +139 more
- 01 Mar 2007 - 
TL;DR: Linkage and copy number variation analyses implicate chromosome 11p12–p13 and neurexins, respectively, among other candidate loci, highlighting glutamate-related genes as promising candidates for contributing to ASDs.
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Correlation Between Elevated Levels of Amyloid β-Peptide in the Brain and Cognitive Decline

TL;DR: An important role for Abeta in mediating initial pathogenic events in AD dementia is supported and treatment strategies targeting the formation, accumulation, or cytotoxic effects of Abeta should be pursued.