Is lead exposure in early life an environmental risk factor for Schizophrenia? Neurobiological connections and testable hypotheses

NeuroToxicology

Volumn 33, Issue 3, 2012, Pages 560-574

  Guilarte, Tomás R ^a   Opler, Mark ^b   Pletnikov, Mikhail ^c  

^a Department of Medicine   (United States)

^b NEW YORK UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

DISC1; Early life; Gene environment interaction; Lead; NMDA receptor; Pb 2+; Schizophrenia

Indexed keywords

3 ALLYL 6 CHLORO 2,3,4,5 TETRAHYDRO 7,8 DIHYDROXY 1 PHENYL 1H 3 BENZAZEPINE; APOMORPHINE; DISRUPTED IN SCHIZOPHRENIA 1 PROTEIN; DIZOCILPINE; DOPAMINE 2 RECEPTOR; KETAMINE; LEAD; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; NEUROLEPTIC AGENT; NICOTINIC RECEPTOR; PHENCYCLIDINE;

AUTOPSY; BEHAVIOR; BRAIN GROWTH; BRAIN LEVEL; BRAIN SIZE; COGNITION; DIFFUSION TENSOR IMAGING; DISC 1 GENE; ENVIRONMENTAL EXPOSURE; ENVIRONMENTAL FACTOR; GENE; GENETIC ASSOCIATION; GENOTYPE ENVIRONMENT INTERACTION; HUMAN; MENTAL DISEASE; NERVE CELL PLASTICITY; NEUROIMAGING; NEUROTOXICITY; NONHUMAN; NUCLEAR MAGNETIC RESONANCE IMAGING; NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY; PRIORITY JOURNAL; REVIEW; RISK ASSESSMENT; SCHIZOPHRENIA;

AGE FACTORS; ANIMALS; APOPTOSIS; DOPAMINE; ENVIRONMENTAL EXPOSURE; ENVIRONMENTAL POLLUTANTS; GAMMA-AMINOBUTYRIC ACID; GENE-ENVIRONMENT INTERACTION; GLUTAMINE; HUMANS; LEAD; LEAD POISONING, NERVOUS SYSTEM; MUTATION; NERVE TISSUE PROTEINS; NEURONS; RECEPTORS, N-METHYL-D-ASPARTATE; RISK ASSESSMENT; RISK FACTORS; SCHIZOPHRENIA; SCHIZOPHRENIC PSYCHOLOGY;

MUS;

EID: 84861199523     PISSN: 0161813X     EISSN: 18729711     Source Type: Journal    
DOI: 10.1016/j.neuro.2011.11.008     Document Type: Review

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