Speeding Brain’s Garbage Disposal Could Slow Alzheimer’s


In the modern neurodegenerative care, scientists have been on the merge in determining the way of treating diseases associated with the brain. Recent researchers from the role of endocannabinoids to cannabinol have proven the possibility of regulating neurogenesis disorders as asserted by Aswin Suri, Chairman of Neuro-Endoceuticals, USA. On the other hand, recent studies have found that using drugs to boost the activity in the brain “garbage disposal” has the potential of removing the toxic protein that clumps together in the brain to cause Alzheimer’s disease. Consequently, Aswin Suri, Chairman of the Neuro-Endoceuticals and Michael Menbrino, President of Neuro-Endoceuticals, USA, argues that most of the neurological disorder such as AD is characterized by the accumulation of protein in the brain, which will result into various tauopathies.

Research conducted by Feunerburk, Marcellino, and Yue (2010) found that overexpression of protein accumulation in the brain has resulted in various autophagy dysfunction. In their investigation, they discovered that the use of different depressant to boost brain through activation of garbage disposal system slows down the disease in mouse model. However, in the study, the team posted that use of different animals, cellular models, and experimental paradigm may provide distinct differences in conclusions (Feunerburk, Marcellino, and Yue, 2010).

Similarly, research conducted by scientists from the University of Columbia have been reported new ways of activating brain garbage disposal system can reduce the prevalence of Alzheimer’s disease. As reported by Karen Duff, the team leader of the research group, use of drugs to increase or speed up the brain garbage disposal system is beneficial in the sense that it open new interventions for treating the disease and several other neurogenesis disorders (Dockrill, 2015).

Focusing on the nature of protein accumulation in the brain, the cells of the brain tend to clear off the dead cells and replace them with new ones. Because these damaged protein cells may sometimes be sticky, for example, amyloid beta and tau proteins, they clot or stick together and contribute to the development of Alzheimer’s disease. In the study, the team used mouse models and administered rolipram that is an antidepressant to the mice. In their result, they discovered that the level of the toxic protein in the brain of the mice was reduced the positive effect. In their explanation, rolipram activated proteasome and restored the protein disposal to normal levels. Additionally, the drug was associated with the improved memory of the mice, but this was unclear (Dockrill, 2015).

Following the recent study, it was discovered that the mechanism to which rolipram works is through the inhibition of the PDE-4 enzyme, which can increase the activity of proteasome within the brain. On the other end, accumulation of the protein in the brain is connected to reduce peptidase activity, which leads to high levels of ubiquitinated proteins. The potential interference of dysfunctional tau with autophagosome clearance may lead to AD neuropathology. This is possible because tau has have been reported to control the stability or microtubules; hence, the modification of tau can lead to stabilization of the condition. Consequently, it was possible that the researchers were able to activate proteasome, which resulted in the reduction of the tau and improvement in memory function of the mice, it was still on how the anti-depressant worked.

Besides, clinical manifestation shows that rolipram can cause nausea and the drug is not advised to be administered to human beings. In effects, the researchers reported that they have no idea of how the rolipram was able to activate the proteasome and regulated the protein accumulation in the brain. However, it was apparent that the team was able to understand and discover that use of some drugs, in this scenario, rolipram was able to stimulate this disposal system in neurons and efficiently reduces the Alzheimer’s disease.

In this light, there is a potential in new interventions of Alzheimer’s disease and other neurodegenerative illnesses. In conclusion, Aswin Suri, Chairman of the Neuro-Endoceuticals and his colleague Mike Membrino, President of Neuro-Endoceuticals, USA, assert that drugs that may act in activation of proteasome can be used to assist in the management of the AD and other protein based accumulation diseases such as Parkinson’s disease, Huntington’s disease, and frontotemporal dementia.

References Dockrill, P. (2015). Drug that Boost the Brain’s “Garbage Disposal” Slows Alzheimer’s in Mice. Colombia University Medical Care. Funderburk, S. F., Marcellino, B. K., & Yue, Z. (2010). Cell “Self-Eating” (Autophagy) Mechanism in Alzheimer’s Disease. The Mount Sinai Journal of Medicine, New York, 77(1), 59–68.

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