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Anna Karydas

Researcher at University of California, San Francisco

Publications -  164
Citations -  19783

Anna Karydas is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Frontotemporal dementia & Frontotemporal lobar degeneration. The author has an hindex of 54, co-authored 158 publications receiving 15901 citations. Previous affiliations of Anna Karydas include Icahn School of Medicine at Mount Sinai & University of California, Davis.

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Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS

Mariely DeJesus-Hernandez, +28 more
- 20 Oct 2011 - 
TL;DR: It is found that repeat expansion in C9ORF72 is a major cause of both FTD and ALS, suggesting multiple disease mechanisms.
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Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease.

Adam C. Naj, +156 more
- 01 May 2011 - 
TL;DR: The Alzheimer Disease Genetics Consortium performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1), two replication stages (stages 2 and 3), and both joint analysis and meta-analysis approaches were used.
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Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteins

Sandip Ray, +25 more
- 01 Nov 2007 - 
TL;DR: Biological analysis of the 18 proteins found in blood plasma points to systemic dysregulation of hematopoiesis, immune responses, apoptosis and neuronal support in presymptomatic Alzheimer's disease.
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Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

Rebecca Sims, +487 more
- 01 Sep 2017 - 
TL;DR: Three new genome-wide significant nonsynonymous variants associated with Alzheimer's disease are observed, providing additional evidence that the microglia-mediated innate immune response contributes directly to the development of Alzheimer's Disease.
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Progranulin Deficiency Promotes Circuit-Specific Synaptic Pruning by Microglia via Complement Activation.

Hansen Lui, +28 more
- 05 May 2016 - 
TL;DR: In this paper, the authors used transcriptome profiling to demonstrate that deficiency in frontotemporal dementia (FTD) gene progranulin (Grn) leads to an age-dependent, progressive upregulation of lysosomal and innate immunity genes, increased complement production, and enhanced synaptic pruning in microglia.