Softcover reprint of the original 1st ed. 1994, X, 201 p.
Springer eBooks may be purchased by end-customers only and are sold without copy protection (DRM free). Instead, all eBooks include personalized watermarks. This means you can read the Springer eBooks across numerous devices such as Laptops, eReaders, and tablets.
You can pay for Springer eBooks with Visa, Mastercard, American Express or Paypal.
After the purchase you can directly download the eBook file or read it online in our Springer eBook Reader. Furthermore your eBook will be stored in your MySpringer account. So you can always re-download your eBooks.
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.
Molecular biology of Huntington's disease. Neuronal pathology in relation to molecular biology and treatment of Alzheimer's disease. The aetiology of Alzheimer's disease. The molecular genetics of Alzheimer's disease. The molecular biology of the transmissible dementias. The neurochemistry of schizophrenia. Molecular biology of shcizophrenia. Genetics and molecular biology of manic-depression. Index.