Connecting Synaptic Gene Polymorphisms to Parkinson’s Disease


Neurodegenerative disorders represent a significant and growing concern in the realm of public health, particularly as global populations age. Among these, Parkinson’s disease (PD) stands out due to its increasing prevalence and profound impact on individuals. Characterized by the progressive degeneration of motor functions, PD is not just a health challenge but also poses substantial socio-economic burdens. While the etiology of Parkinson’s disease is far from simple, current research efforts elucidating its causes, mechanisms, and potential treatments illustrate the critical nature of this neurodegenerative disorder in today’s healthcare landscape.

In the clinic, Parkinson’s disease is often diagnosed as either sporadic or familial. Familial PD has a clear genetic basis, typically passed down through families, while sporadic PD, comprising about 90% of cases, occurs in individuals without a known family history of the disease. The exact cause of sporadic PD is not fully understood but is believed to be due to a combination of genetic predispositions and environmental factors. In contrast, the factors involved in familial PD are more thoroughly understood, offering insights into the molecular mechanisms underlying PD pathogenesis.

Polymorphisms and Parkinson’s Disease Susceptibility

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Dyed cells live longer?

When I first came across an article about methylene blue being protective against neuronal death, I was intrigued. I had always associated methylene blue (sometimes confused with methyl blue—an entirely different molecule) with staining nucleic acids or proteins following membrane transfer or with staining bacteria or its use as a redox indicator. It turns out that methylene blue (MB) has an extremely wide range of applications: commercial (dye in the textile / paper industry), laboratory (supravital dye, redox indicator) and an amazingly large plethora of clinical and therapeutic (early Alzheimer’s disease, mild cognitive impairment) applications(1). In fact, MB is an FDA-grandfathered antidote for the treatment of methemoglobinemia, a condition characterized by elevated levels of oxidized form of hemoglobin that interferes with its ability to release oxygen to the tissues.

What makes this compound, so rightly called “magic bullet” so unique and versatile? Continue reading “Dyed cells live longer?”

Hypomethylation in the Hippocampus: Can Age-Related Cognitive Decline in Mice Be Reversed by the Activity of One Gene?

Partial ribbon structure of DNMT3a Source: Protein Database
Buried in the middle of the August issue of Nature Neuroscience is an article (1) by Oliveira, Hemstedt and Bading that caught my eye. It isn’t often that I see a paper about gene rescue in a neuroscience journal, especially in a study about cognitive decline.

I looked for a News and Views summary of the article, thinking that if the conclusions of the article were anything like what the title and abstract indicated, there must be an editorial summary. I wasn’t disappointed. Su and Tsai provided a nice summary of the paper and discussed some of the potential implications of the work (2). Continue reading “Hypomethylation in the Hippocampus: Can Age-Related Cognitive Decline in Mice Be Reversed by the Activity of One Gene?”