PMID: 9729369Sep 5, 1998Paper

Orphan neurones and amine excess: the functional neuropathology of Parkinsonism and neuropsychiatric disease

Brain Research. Brain Research Reviews
G L Willis, S M Armstrong


The aetiology and treatment of Parkinsonism is currently conceptualised within a dopamine (DA) deficiency-repletion framework. Loss of striatal DA is thought to cause motor impairment of which tremor, bradykinaesia and rigidity are prominent features. Repletion of deficient DA should at least minimise parkinsonian signs and symptoms. In Section 2, based on extensive pre-clinical and clinical findings, the instability of this approach to Parkinsonism is scrutinised as the existing negative findings challenging the DA deficiency hypothesis are reviewed and reinterpreted. In Section 3 it is suggested that Parkinsonism is due to a DA excess far from the striatum in the area of the posterior lateral hypothalamus (PLH) and the substantia nigra (SN). This unique area, around the diencephalon/mesencephalon border (DCMCB), is packed with many ascending and descending fibres which undergo functional transformation during degeneration, collectively labelled 'orphan neurones'. These malformed cells remain functional resulting in pathological release of transmitter and perpetual neurotoxicity. Orphan neurone formation is commonly observed in the PLH of animals and in man exhibiting Parkinsonism. The mechanism by which orphan neurones impair...Continue Reading


Nov 1, 1977·Psychological Medicine·A Carlsson
Mar 14, 1978·Biochimica Et Biophysica Acta·T NagatsuM Akino
Jan 1, 1979·Psychoneuroendocrinology·D P van Kammen
Dec 1, 1979·The British Journal of Psychiatry : the Journal of Mental Science·D N BatemanM D Rawlins
May 1, 1977·Physiology & Behavior·T A Schoenfeld, L W Hamilton
Aug 1, 1976·Neurology·B B MrsuljaI Klatzo
Nov 1, 1976·Journal of Neurology, Neurosurgery, and Psychiatry·A H Rajput, B Rozdilsky
Sep 29, 1978·Biochemical and Biophysical Research Communications·C C FelixR C Sealy
Dec 29, 1978·Brain Research·R Govrin-Lippmann, M Devor
May 1, 1979·Brain Research Bulletin·P A van DongenA R Cools
May 15, 1975·Biochemical Pharmacology·O Hornykiewicz
Nov 1, 1977·Brain Research Bulletin·G Singer, G L Willis
Jan 1, 1979·Acta Psychiatrica Scandinavica·J A Yaryura-Tobias
Jan 1, 1978·Acta Neurologica Scandinavica·A C PetersG T Bots
May 5, 1978·Science·C A TammingaJ M Davis
Feb 1, 1978·Annals of Neurology·J W Langston, L S Forno
Jun 22, 1979·Brain Research·D T MasuokaC E Finch
Feb 1, 1979·Journal of Comparative and Physiological Psychology·J S Fink, G P Smith
Oct 26, 1979·Science·S G PotkinR J Wyatt
Mar 1, 1977·Pharmacology, Biochemistry, and Behavior·G F AlheidS P Grossman
May 1, 1979·Pharmacology, Biochemistry, and Behavior·G K Hodge, L L Butcher
Feb 20, 1978·Acta Neuropathologica·K JellingerP Kothbauer
Mar 1, 1978·Biochemical Pharmacology·P C Waldmeier, A E Felner
Dec 1, 1978·British Journal of Clinical Pharmacology·G P ReynoldsG M Stern
Jan 1, 1978·Journal of Neural Transmission·J Knoll

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Jul 15, 1999·Physiology & Behavior·G L Willis, S M Armstrong
May 27, 2008·Brain Research·Gregory L Willis
Feb 13, 2001·The Journal of Comparative Neurology·K A MesceK A Klukas

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