[The neurochemistry and neuropharmacology of diffuse Lewy body disease]

Rev Neurol. 2006 May;42(9):549-55.
[Article in Spanish]

Abstract

Introduction and development: The main neurochemical alteration in diffuse Lewy body disease (DLBD) is the cholinergic deficit in the cerebral cortex, which involves mainly cholin-acetyl-transferase. There have been also described dopamine deficiency and alterations affecting other neurotransmitters and neuromodulators, such as serotonin, noradrenaline, neuropeptides, etc. Cerebral perfusion and glucose metabolism studies usually show diffuse hypoperfusion or hypometabolism, with higher alteration of associative cortex, including occipital involvement. Several studies have shown increased markers of oxidative stress in brain and other tissues, suggesting its possible role in the pathogenesis of DLBD.

Conclusions: Acetylcholinesterase inhibitors seem to improve cognitive and conductual symptoms, although their usefulness according evidence-based medicine criteria is weak. Some patients need atypical neuroleptics at low doses to get the symptomatic control of conductual alterations.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Acetylcholine / chemistry*
  • Acetylcholine / metabolism
  • Brain Chemistry*
  • Cerebrovascular Circulation
  • Choline O-Acetyltransferase / chemistry
  • Choline O-Acetyltransferase / metabolism
  • Cholinesterase Inhibitors / therapeutic use
  • Humans
  • Lewy Body Disease / drug therapy
  • Lewy Body Disease / physiopathology*
  • Oxidative Stress

Substances

  • Cholinesterase Inhibitors
  • Choline O-Acetyltransferase
  • Acetylcholine