•  
  •  
 

Eukaryon

Class Year

2007

Keywords

Parkinson’s Disease Etiology, movement disorder, oxidative stress, Dopamine auto-oxidation, mitochondrial dysfunction, non-electron transport deficiencies

Abstract

Parkinson’s disease (PD) affects over 500,000 Americans. Most cases of PD are idiopathic, or occurring without a known cause. Two pathological features of PD, á-synuclein-rich Lewy bodies (LB) and oxidative damage, hint at the cause of the disease. Yet, disparities in recessive forms of PD increase the complexity of the disease mechanism. These recessive forms occur earlier in life and are devoid of LB. One common feature among these forms is the extensive presence of reactive oxygen species (ROS). Studies with the toxin MPTP produced similar pathologies to recessive PD but intriguingly showed inhibition of complex I in the mitochondria. These and other studies chased the mitochondria as the progenitor of oxidative stress. These investigations also uncovered several disparate mitochondrial proteins, one of which is a Kreb’s cycle enzyme, α-ketoglutarate dehydrogenase (α-KGDH). Interestingly, α-KGDH activity is reduced in both Alzheimer’s disease (AD) and PD. Links to both diseases may be due to its role in the inactivation of complex I. This review will focus on how mitochondrial impairments enhance neuronal toxicity in PD.

Disclaimer

Eukaryon is published by students at Lake Forest College, who are solely responsible for its content. The views expressed in Eukaryon do not necessarily reflect those of the College. Articles published within Eukaryon should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Share

COinS