Molecular and Cell Biology of Neuropsychiatric Diseases

Name: Molecular and Cell Biology of Neuropsychiatric Diseases
Brand: Springer
SKU: 9789401043052
Price: 7267.0 INR
Availability: InStock

by F. Owen

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ISBN13: 9789401043052
Binding: Paperback
Subject: N/A
Publisher: Springer
Publisher Imprint: Springer
Publication Date: October 28, 2012
Pages: 201
Original Price: EUR 99.99
Language: English
Edition: Softcover Repri
Item Weight: 333 grams
BISAC Subject(s): Neurology, Neuroscience, and Life Sciences / Anatomy & Physiology

About The Book

is''0l m 5-HT Ante-mortem (m = metabolite) . ". Post-mortem m 0 Noradrenaline, -'-'-'-'0-J, -'-'-'-'-'-'- m Dopamine . '-'-'-'-'- . " Somatostatin . '1 Plaques Tangles * . ". . ". . 'I Synapse loss * ChAT " ACh synthesis l"-, . '-'-'-'-'-'-'-'-'-'-'-'-'-, -'-'-'-'-'-'-'-'-'-'-'-'-'-'- * Neuronal loss, -, - . ". * o 0. 1 0. 2 0. 3 0. 4 0. 5 0. 6 0. 7 0. 8 0. 9 1. 0 Correlation coefficient with dementia rating Figure 2. 1 Various neurotransmitter and neuropathological measures on neocortex obtained either at diagnostic craniotomy (ante-mortem) or post-mortem and re- lationship to cognitive impairment (dementia rating). Asterisks identify significant correlations. Negative and positive correlations are not identified in this represen- tation of the data. Only the physiologically relevant measure of cholinergic neurones (acetylcholine synthesis) and indices of cortical pyramidal neurone degeneration (neuronal loss, synapse loss and tangles) correlate with severity of dementia. Note the lack of correlation with the structural marker of cholinergic neurones, ChAT activity. Loss of enzyme exceeded that of acetylcholine synthesis (Sims et al., 1983a), suggesting a compensatory increase in synthesis in the few remaining neurones. Data derived from Palmer (1987) and Terry et al. (1991). emission tomography (PET) and magnetic resonance, may some day pro- vide routine insight into differences in brain functioning. Success in developing rapid and reliable diagnostic procedures, perhaps based on changes in body fluid that reflect specific alterations in brain protein metabolism, should ultimately play an important role in the clinical development of new therapeutic agents.

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