Alzheimer’s disease, the most common neurodegenerative disorder of adults since it creates a problem with memory, thinking, and behavior. It remains unbeknownst and requires more concentration to observe the intracellular aspects in view of the mentioned disease. The key event in developing the disorder is the formation of amyloid-beta protein, which accumulates to form amyloid plaques in the neurons.
The study
Researchers from the Tufts University School of Medicine found the molecular mechanism underlying the cause of Alzheimer’s. It was primarily due to the enzyme BACE1, as this provides the amyloid plaque to cluster inside the axons.
Beta-site APP cleaving enzyme 1 (BACE1)
The BACE1 is an enzyme that is primarily responsible for generating amyloid plague. The knock out of this gene does not produce any beta-amyloid and are free from Alzheimer’s associated pathologies. The gene mutation altogether enhances the expression of the gene, happened with the African Americans, and is much affected due to traffic jam of the enzyme BACE1 in axons.
A person exhibits the symptoms only after 20 years since the initial stages begin in the neuron. Therefore, identifying the mutation will definitely assist in early treatment and perhaps prevent delayed outcomes.
Earlier study
The same researchers already described the Gga3 gene, that regulates the expression of BACE1. When the Gga3 gene knocked out from the mice, they observed a significant increase in the amyloid plaques in the axons leading to swelling. According to the data from the National Institute of Mental Health and the Alzheimer’s Disease Neuroimaging Initiative, the African Americans had Gga3 mutation and so developed AD later.
Could the BACE1 inhibitors stop Alzheimer’s?
When it comes to delayed or advanced disease where the amyloid clusters are drastically more in the neurons, the treatments with BACE1 inhibitors are not much effective. Nonetheless, the researchers said that the use of these inhibitors would definitely help at the earliest stage. They claimed that there was a reduction in the swelling of axons, thereby preventing the progression of the disorder.
Pharmacological inhibition of BACE prevents the formation of AD-like pathology in cultured neurons and in the mouse brain
To conclude, the study showed the molecular aspects that affect earlier, which would indicate the diagnosis of the disease. Also, a lot more research on the therapeutic aspect of the BACE1 inhibitors is highly favored in the coming years.
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Source: MedicalXpress
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