Amine accumulation in Parkinson's disease and other disorders

Abstract

Amine accumulation in the axons of degenerating, amine-containing neurones is a natural component of neurone death in many species, including man. While it is becoming increasingly clear that this phenomenon may have functional significance in animal models of Parkinson's Disease, its potential importance in the clinical syndrome has been pretermitted. There are several reasons for this. Failure to sample tissue which contains accumulated amines, the masking of accumulation by adjacent depleted tissues and the degradation of accumulated amines in post-mortem tissues from Parkinsonian brains could account for the low incidence of detection of accumulation in this disorder. Increased levels of amines have been detected in the brains of patients with other conditions including cerebral infarction, Alzheimer's Disease and Huntington's Chorea. These increases have been attributed previously to enhanced aminergic activity, rather than a stage in the degenerative process, as our hypothesis suggests. In addition to the potential importance of amine accumulation in the pathophysiology of various clinical syndromes, a more thorough investigation of this phenomenon in animal models would seem essential since they are used routinely to both describe the basic principles of dopamine function and to evaluate therapeutic possibilities in Parkinson's Disease.