title: An aspect of Alzheimer neuropathology after suicide transport damage.
abstract: Concentrations of APP-like immunoreactivity have been determined by western blotting in a soluble fraction and two membrane fractions of brain cortex from demented patients (14 with Alzheimer's disease and 8 with other diagnoses). The concentration of APP in the soluble fraction correlated with the number of pyramidal neurones but not astrocytes or indices of interneurones. Experimental lesions in rats and quantitative autoradiography were used to investigate the cellular localisation of receptors. Lesions were produced by intrastriatal or intracortical injections of volkensin to destroy corticofugal and corticortical pyramidal neurons respectively. Volkensin treatment caused significant loss of pyramidal neurones which was accompanied by reduced binding to muscarinic cholinergic m1 receptors. [3H] 8-OH-DPAT (serotonin 1A receptors) binding was reduced only following intrastriatal volkensin. Results from the human and rat investigations are discussed in terms of the biology of cortical pyramidal neurones and drugs for the treatment of Alzheimer's disease.
authors.affiliation: Miriam Marks Department of Neurochemistry, Institute of Neurology, London, United Kingdom.
authors.forename: I P
authors.initials: IP
authors.lastname: Chessell
authors.forename: P T
authors.initials: PT
authors.lastname: Francis
authors.forename: M T
authors.initials: MT
authors.lastname: Webster
authors.forename: A W
authors.initials: AW
authors.lastname: Procter
authors.forename: P R
authors.initials: PR
authors.lastname: Heath
authors.forename: R C
authors.initials: RC
authors.lastname: Pearson
authors.forename: D M
authors.initials: DM
authors.lastname: Bowen
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006023:Glycoproteins; D008297:Male; D009699:N-Glycosyl Hydrolases; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D037121:Plant Lectins; D010940:Plant Proteins / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar; D011941:Receptors, Adrenergic / Q000378:metabolism; D017982:Receptors, Biogenic Amine; D011963:Receptors, GABA-A / Q000378:metabolism; D018092:Kainic Acid Receptors / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D011978:Receptors, Nicotinic / Q000378:metabolism; D018047:Receptors, Purinergic P1 / Q000378:metabolism; D011985:Receptors, Serotonin / Q000378:metabolism; D054790:Ribosome Inactivating Proteins, Type 2; D014118:Toxins, Biological
chemical_list: D006023:Glycoproteins; D009699:N-Glycosyl Hydrolases; D037121:Plant Lectins; D010940:Plant Proteins; D011941:Receptors, Adrenergic; D017982:Receptors, Biogenic Amine; D011963:Receptors, GABA-A; D018092:Kainic Acid Receptors; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D011978:Receptors, Nicotinic; D018047:Receptors, Purinergic P1; D011985:Receptors, Serotonin; D054790:Ribosome Inactivating Proteins, Type 2; D014118:Toxins, Biological; C049134:volkensin