Professional Information
- Profession
- Researcher / Scientist
- Specialty/Area of Focus
- Genes, risk factors , particularly viruses and pathogens in human disease
- Bio
- See linked in profile at http://www.linkedin.com/pub/chris-carter/22/560/76a
Social Media and Site Links
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http://www.polygenicpathways.co.uk
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ADHD genes and risk factors
Autism genes and risk factors
Chronicfatigue fibromyalgia risk factors
Alzheimer's genes and risk factors
Depression genes and risk factors
Schizophrenia genes and risk factors
Bipolar disorder genes and risk factors
Herpes simplex life cycle
Parkinson's disease genes and risk factors
Anorexia genes and risk factors
Childhood obesity genes and risk factors
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Profile Details
- Location
- UK
- Honorifics
- B.Sc, M.Sc, PhD
- Languages
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English (Native fluency)
French (Professional fluency)
- Schools
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University of Leeds: 1971-1974
B.Sc Zoology
Bacteriology, parasitology, physiology, ecology, marine biology, population genetics
University of Bradford: 1975-1976
M.Sc Pharmacology and Toxicology
University of Bristol: 1976-1979
Ph.D
Neuropharmacology
- Publications
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Vaccinia and other viruses with available vaccines show marked homology with the HIV-1 envelope glycoprotein: The prospect of using existing vaccines to stem the AIDS pandemic.Immunopharmacol Immunotoxicol. | 2011
Authors: C.J.CarterSmallpox vaccination has been shown to reduce HIV-1 viral load in vitro and certain other viruses also limit HIV-1 infection. This may be due to extensive protein sequence similarities between these viruses: A resumption of smallpox vaccination could perhaps diminish AIDS
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 DiseaseISRN:Neurology | 2011
Authors: C.J.CarterMany of the environmental risk factors in Alzheimer's disease are able to provoke beta-amyloid deposition and also herpes simplex reactivation. Each risk factor can be related to subsets of susceptibility genes suggesting that the risk factors are in fact causes, whose effects are conditioned by the genes. Many of these causes are preventable by simple measures such as diet, vitamin supplementation and pathogen detection and elimination.
Toxoplasmosis and Polygenic Disease Susceptibility Genes: Extensive Toxoplasma gondii Host/Pathogen Interactome Enrichment in Nine Psychiatric or Neurological DisordersJ.Pathogens | 2013
Authors: C.J.CarterToxoplasma gondii, is implicated in schizophrenia and related disorders, but also in Alzheimer’s or Parkinson’s disease, cancer, cardiac myopathies, and autoimmune disorders. During its life cycle, the pathogen interacts with ~3000 host genes or proteins. Susceptibility genes for multiple sclerosis > Alzheimer’s disease > schizophrenia > bipolar disorder> depression > childhood obesity > Parkinson’s disease > attention deficit hyperactivity disorder (P from 8.01E-05 (ADHD) to 1.22E-71 (multiple sclerosis), and autism (p=0.013), but not anorexia or chronic fatigue are highly enriched in the human arm of this interactome and 18 (ADHD) to 33% (MS) of the susceptibility genes relate to it. The signalling pathways involved in the susceptibility gene/interactome overlaps are relatively specific and relevant to each disease suggesting a means whereby susceptibility genes could orient the attentions of a single pathogen towards disruption of the specific pathways that together contribute (positively or negatively) to the endophenotypes of different diseases. Conditional protein knockdown, orchestrated by T. gondii proteins or antibodies binding to those of the host (pathogen derived autoimmunity) and metabolite exchange, may contribute to this disruption. Susceptibility genes may thus be related to the causes and influencers of disease, rather than (and as well as) to the disease itself.
Convergence of genes implicated in Alzheimer's disease on the cerebral cholesterol shuttle: APP, cholesterol, lipoproteins, and atherosclerosis.Neurochem. Int | 2007
Authors: C.J.CarterPolymorphic genes associated with Alzheimer's disease (see ) delineate a clearly defined pathway related to cerebral and peripheral cholesterol and lipoprotein homoeostasis. They include all of the key components of a glia/neurone cholesterol shuttle including cholesterol binding lipoproteins APOA1, APOA4, APOC1, APOC2, APOC3, APOD, APOE and LPA, cholesterol transporters ABCA1, ABCA2, lipoprotein receptors LDLR, LRP1, LRP8 and VLDLR, and the cholesterol metabolising enzymes CYP46A1 and CH25H, whose oxysterol products activate the liver X receptor NR1H2 and are metabolised to esters by SOAT1. LIPA metabolises cholesterol esters, which are transported by the cholesteryl ester transport protein CETP. The transcription factor SREBF1 controls the expression of most enzymes of cholesterol synthesis. APP is involved in this shuttle as it metabolises cholesterol to 7-betahydroxycholesterol, a substrate of SOAT1 and HSD11B1, binds to APOE and is tethered to LRP1 via APPB1, APBB2 and APBB3 at the cytoplasmic domain and via LRPAP1 at the extracellular domain. APP cleavage products are also able to prevent cholesterol binding to APOE. BACE cleaves both APP and LRP1. Gamma-secretase (PSEN1, PSEN2, NCSTN) cleaves LRP1 and LRP8 as well as APP and their degradation products control transcription factor TFCP2, which regulates thymidylate synthase (TS) and GSK3B expression. GSK3B is known to phosphorylate the microtubule protein tau (MAPT). Dysfunction of this cascade, carved out by genes implicated in Alzheimer's disease, may play a major role in its pathology. Many other genes associated with Alzheimer's disease affect cholesterol or lipoprotein function and/or have also been implicated in atherosclerosis, a feature of Alzheimer's disease, and this duality may well explain the close links between vascular and cerebral pathology in Alzheimer's disease. The definition of many of these genes as risk factors is highly contested. However, when polymorphic susceptibility genes belong to the same signaling pathway, the risk associated with multigenic disease is better related to the integrated effects of multiple polymorphisms of genes within the same pathway than to variants in any single gene [Wu, X., Gu, J., Grossman, H.B., Amos, C.I., Etzel, C., Huang, M., Zhang, Q., Millikan, R.E., Lerner, S., Dinney, C.P., Spitz, M.R., 2006. Bladder cancer predisposition: a multigenic approach to DNA-repair and cell-cycle-control genes. Am. J. Hum. Genet. 78, 464-479.]. Thus, the fact that Alzheimer's disease susceptibility genes converge on a clearly defined signaling network has important implications for genetic association studies.
- Site Groups
- Medical Technology, Pharmacist, PhD, Doctor
