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Home: Community: Researcher Profiles
Researcher Profile

RESEARCHER INFORMATION
First Name:Chris
Last Name:Carter
Title:Dr
Advanced Degrees:B.Sc, M.Sc, PhD
Affiliation:PolygenicPathways
Country/Territory:United Kingdom
Email Address: 
Disclosure:
(view policy) 
Member reports no financial or other potential conflicts of interest. [Last Modified: 10 September 2011]
View all comments by Chris Carter
Clinical Interests:
Alzheimer Disease, Parkinson Disease, Aging Process, Stroke and Trauma, Polyglutamine Disorders (Huntington's, etc.)
Research Focus:
DNA microarrays, virology, Epidemiology, Neuroimmunology, Neuropathology, Neurobiology, Chemistry/Pharmacology, Bioinformatics/Statistics, Genetics
Work Sector(s):
Private
Web Sites:
Personal: http://polygenicpathways.blogspot.com/
Professional: http://www.polygenicpathways.co.uk
Researcher Bio
I started off in Neuroscience with an M.Sc with Brenda Costall and Robert Naylor who fuelled an interest in dopamine that I continued with a PhD with Chris Pycock at Bristol, leading to some useful work on dopamine in the frontal cortex. I obtained fellowships from the Parkinson' disease society and the Huntington's disease association and spent postdoctoral time in David Marsden's Neurology department at the Institute of Psychiatry.This was spent looking at the biochemistry of post-mortem brains, showing reduced glutamine synthetase and other metabolic changes in HD, and evidence for free radical damage in the substantia nigra in Parkinson's disease.
From there to industry with Synthelabo in Paris , ending up as head of the Neuroscience Genomics group in what had become Sanofi-Aventis.
I now work from home trying to make sense of the multiple interactions between genes and risk factors in polygenic diseases. I also run a website which collects such information.
Top Papers
Carter C.J. Alzheimer’s disease: APP, gamma secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1 and MS4A2, and their relationships with herpes simplex , C.Pneumoniae, other suspect pathogens and the immune system:Int J.Alz.Dis, 2011 http://www.hindawi.com/journals/ijad/aip/501862/

Carter, C.J. The fox and the rabbits, environmental variables and population genetics.1: Replication problems in association studies and the untapped power of GWAS. 2: Vitamin A deficiency, herpes simplex reactivation and other causes of Alzheimer’s disease ISRN Neurology, 2011, in press http://www.hindawi.com/isrn/neurology/aip/394678/

Carter, C.J. Alzheimer's Disease: A Pathogenetic Autoimmune Disorder Caused by Herpes Simplex in a Gene-Dependent Manner: International Journal of Alzheimer's Disease (2010) http://www.sage-hindawi.com/journals/ijad/2010/140539.html#B54

Carter C.J. Alzheimer's disease plaques and tangles: Cemeteries of a Pyrrhic victory of the immune defence network against herpes simplex infection at the expense of complement and inflammation-mediated neuronal destruction.

Neurochem Int. 2010 Dec 15 (http://www.polygenicpathways.co.uk/platang.htm)

APP, APOE, Complement receptor 1, Clusterin and PICALM and their involvement in the Herpes simplex life-cycle.
Neurosci Lett. 2010 Jul 29 epub
PMID:20674675
http://www.ncbi.nlm.nih.gov/pubmed/20674675

Schizophrenia susceptibility genes directly implicated in the life cycles of pathogens: cytomegalovirus, influenza, herpes simplex, rubella, and Toxoplasma gondii.
Schizophr Bull. 2009 Nov;35(6):1163-82
PMID: 18552348
http://www.ncbi.nlm.nih.gov/pubmed/18552348

Interactions between the products of the Herpes simplex genome and Alzheimer's disease susceptibility genes: Relevance to pathological-signalling cascades.
Neurochem Int. 2008 52(6):920-34.
PMID: 18164103
http://www.ncbi.nlm.nih.gov/pubmed/18164103

Carter CJ.
Convergence of genes implicated in Alzheimer's disease on the cerebral cholesterol shuttle: APP, cholesterol, lipoproteins, and atherosclerosis.
Neurochem Int. 2007 Jan;50(1):12-38.
PMID: 16973241
http://www.ncbi.nlm.nih.gov/pubmed/16973241

Carter CJ.
eIF2B and oligodendrocyte survival: where nature and nurture meet in bipolar disorder and schizophrenia?
Schizophr Bull. 2007 Nov;33(6):1343-53
PMID: 17329232
http://www.ncbi.nlm.nih.gov/pubmed/17329232

Carter CJ. Multiple genes and factors associated with bipolar disorder converge on growth factor and stress activated kinase pathways controlling translation initiation: implications for oligodendrocyte viability. Neurochem Int. 2007 Feb;50(3):461-90.
PMID: 17239488

Carter CJ.Schizophrenia susceptibility genes converge on interlinked pathways related to glutamatergic transmission and long-term potentiation, oxidative stress and oligodendrocyte viability.
Schizophr Res. 2006 Sep;86(1-3):1-14.
PMID:16842972
http://www.ncbi.nlm.nih.gov/pubmed/16842972
What is the greatest void to date in our knowledge of Alzheimer's Disease?
How genes and risk factors act together to condition each other's effects.
What are the top three papers (not yours) you have read recently?
Antibodies in Alzheimer's disease

http://www.utsouthwestern.edu/utsw/cda/dept353744/files/628149.html
What is your leading hypothesis?
Genes and environmental risk factors condition each other's effects and together cause disease.
What piece of missing evidence would help prove it?
Partitioning GWAS data with respect to everything measureable in the same blood samples or other variables: e.g. HDL, LDL, vitamins, autoantibodies, pathogens, aluminium etc etc...........

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