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

Abstract

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

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Citations

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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