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Lecithin in Parkinson’s Disease

  • A. Barbeau
Part of the Journal of Neural Transmission book series (NEURAL SUPPL, volume 16)

Summary

Pathological and biochemical evidence reviewed favours the hypothesis that the dementia seen in Parkinson’s disease, particularly after long-term levodopa therapy, is akin to Alzheimer’s disease. We postulate, in late Parkinson’s disease, the development of a relative cholinergic deficiency due to the accelerated process of aging and the presence of neurofibrillary tangles (with choline acetyl transferase deficiency). This process would be enhanced by the imbalance in favour of dopaminergic predominance caused by chronic levodopa therapy, and would partially explain the increase in dementia. As a test of this hypothesis we have given 10 levodopa-treated parkinsonian patients with dementia, a regimen of lecithin (average 20 gms/day). A clear improvement in Kohs block design test of constructive ability was noted with a decrease in the toxic symptoms of confusion, hallucinations and nightmares. In another study lecithin produced a decrease in levodopa-induced abnormal movements, but at the expense of motor Performance. These preliminary investigations indicate that the progressive dementia of Parkinson’s disease may not be irreversible.

Keywords

Locus Coeruleus Neurofibrillary Tangle Dentate Nucleus Choline Chloride Cortical Atrophy 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag 1980

Authors and Affiliations

  • A. Barbeau
    • 1
  1. 1.Clinical Research InstituteMontreal, QuebecCanada

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