What causes Parkinsons Disease

What causes Parkinsons Disease? 

Although Parkinsons Disease was first described by James Parkinson in 1817, its cause is still unknown.

The recognition that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) can produce in humans and nonhuman primates a parkinsonian syndrome very similar to Parkinsons Disease led to the hypothesis that an MPTP-like substance in the environment could cause Parkinsons Disease.

One of the theories about the cause of Parkinsons Disease is that, as a result of a defective antioxidant system and increased formation of highly reactive and toxic-free oxygen radicals (oxidative stress), abnormally folded proteins accumulate in the affected neurons and overwhelm the ubiquitin–proteasome system.

When the compensatory autophagic mechanisms fail, intracytoplasmic neuronal inclusions called Lewy bodies form, and the neuron eventually dies.

A growing body of evidence supports the role of genetics in the etiology of Parkinsons Disease.

Families with an autosomal dominant and recessive transmission of otherwise typical Parkinsons Disease have been described, as have monozygotic twins concordant for the disease.

In addition to several monogenetic causes of Parkinsons Disease, such as mutations in genes that code for alpha-synuclein, leucine-rich repeat kinase 2, Parkin, and others, there are other genetic abnormalities that increase vulnerability to cell death, including glucocerebrosidase, particularly common in people of Jewish and Middle Eastern origin.

The etiology of Parkinsons Disease is still speculative, but a combination of environmental factors may be associated with a genetic predisposition.

In addition, there is growing evidence that Parkinsons Disease pathology, particularly accumulation and aggregation of toxic alpha-synuclein, originates in the peripheral system and then spreads from the caudal brainstem rostrally via a prion-like mechanism.

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