Candidate gene association studies of the α4 (CHRNA4) and β2 (CHRNB2) neuronal nicotinic acetylcholine receptor subunit genes in Alzheimer's disease

[1]  Simon M Laws,et al.  Expanding the association between the APOE gene and the risk of Alzheimer's disease: possible roles for APOE promoter polymorphisms and alterations in APOE transcription , 2003, Journal of neurochemistry.

[2]  E. Green,et al.  Are interleukin-1 gene polymorphisms risk factors or disease modifiers in AD? , 2002, Neurology.

[3]  P. Chapman,et al.  Genes, models and Alzheimer's disease. , 2001, Trends in genetics : TIG.

[4]  D. Selkoe Alzheimer's disease: genes, proteins, and therapy. , 2001, Physiological reviews.

[5]  P. Sullivan,et al.  Haplotypes of four novel single nucleotide polymorphisms in the nicotinic acetylcholine receptor beta2-subunit (CHRNB2) gene show no association with smoking initiation or nicotine dependence. , 2000, American journal of medical genetics.

[6]  D. Easton,et al.  The ACE gene and Alzheimer's disease susceptibility , 2000, Journal of medical genetics.

[7]  A. Nordberg,et al.  Decreased Protein Levels of Nicotinic Receptor Subunits in the Hippocampus and Temporal Cortex of Patients with Alzheimer’s Disease , 2000, Journal of neurochemistry.

[8]  E. Perry,et al.  α4 but Not α3 and α7 Nicotinic Acetylcholine Receptor Subunits Are Lost from the Temporal Cortex in Alzheimer's Disease , 1999 .

[9]  H. Schröder,et al.  Mutation screening of the CHRNA4 and CHRNB2 nicotinic cholinergic receptor genes in Alzheimer's disease. , 1999, Neuroreport.

[10]  H. Eisenberg,et al.  Expression of nicotinic acetylcholine receptor subunits in the cerebral cortex in Alzheimer’s disease: histotopographical correlation with amyloid plaques and hyperphosphorylated‐tau protein , 1999, The European journal of neuroscience.

[11]  D. Easton,et al.  Apolipoprotein E Genetic Variation and Alzheimer’s Disease , 1999, Dementia and Geriatric Cognitive Disorders.

[12]  J. Changeux,et al.  Increased neurodegeneration during ageing in mice lacking high‐affinity nicotine receptors , 1999, The EMBO journal.

[13]  G. Wilcock,et al.  The cholinergic hypothesis of Alzheimer’s disease: a review of progress , 1999, Journal of neurology, neurosurgery, and psychiatry.

[14]  S. Shimohama,et al.  Stimulation of α4β2 nicotinic acetylcholine receptors inhibits β-amyloid toxicity , 1998, Brain Research.

[15]  H. Tohgi,et al.  Age-related changes in nicotinic acetylcholine receptor subunits α4 and β2 messenger RNA expression in postmortem human frontal cortex and hippocampus , 1998, Neuroscience Letters.

[16]  S. Shimohama,et al.  Nicotinic receptor stimulation protects neurons against β‐amyloid toxicity , 1997 .

[17]  O. Steinlein,et al.  Possible association of a silent polymorphism in the neuronal nicotinic acetylcholine receptor subunit alpha4 with common idiopathic generalized epilepsies. , 1997, American journal of medical genetics.

[18]  A. Nordberg,et al.  Epibatidine and ABT 418 reveal selective losses of α4β2 nicotinic receptors in Alzheimer brains , 1995 .

[19]  M. Folstein,et al.  Clinical diagnosis of Alzheimer's disease , 1984, Neurology.

[20]  R. Bartus,et al.  The cholinergic hypothesis of geriatric memory dysfunction. , 1982, Science.

[21]  S. Folstein,et al.  "Mini-mental state". A practical method for grading the cognitive state of patients for the clinician. , 1975, Journal of psychiatric research.