2 known isoenzymes of Aldehyde dehydrogenase
(ALDH), ALDH 1A1 and ALDH 2, are found to have the crucial role for
metabolizing toxic amine-related aldehydes and superoxides, to prevent the
destruction of neurons.
Although little is known about their role in
Parkinson’s disease however recent studies conducted show that there are
alterations of ALDH 1A1expression in the brain (substantia nigra) of
individuals with Parkinson’s disease. The level of activity of ALDH 2 was also
found to be abnormal in patients suffering the disease. Scientists are
currently doing more research on the basis of the unusual ALDH activity in
patients with Parkinson’s disease in hope that it could become the solution for
improved and more accurate diagnosis of the disease.

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ReplyDeleteHi Ben & Daniel!^^
ReplyDeleteJust to clarify, when you mention that there are alterations of ALDH 1A1 expression in the brain, does this mean that there is not enough of this aldehyde dehydrogenase to metabolize the toxic amine-related aldehydes & superoxides, thus this destroys the neurons?
By the way, the fun facts are really interesting!:)
Thanks! :)
Supp Danesha! Yes, you are absolutely right. There is a decrease in the expression of ALDH 1A1 in the brain which leads to the increase in reactive toxic molecules and thus the cellular degradation.
DeleteOkay thank you!! ^^
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ReplyDeleteHey guys,
ReplyDeleteJust wondering about something, in one of the previous posts you mentioned that the lack of substrates can cause toxic superoxides to form. With a functional aldehyde dehydrogenase, will the lack of substrates still cause the destruction of the neurons and exacerbate Parkinsons disease through production of superoxides, or will the functional aldehyde dehydrogenase slow the development of Parkinsons from the lack of a dopamine producing substrate?
Thanks,
Zheng Jie
Supp Zheng Jie! The toxic superoxides formed can be metabolized by functional aldehyde dehydrogenase, however patients with Parkinson's disease are often associated with low or even absence of ALDH 1A1 expression in their brain. Hence the disease will continue to progress.
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