Plaques formed in the brain are the main culprits that cause Alzheimer's disease (AD).
Plaques - These are the unique structures in the brain tissue that are suspected to be involved during the development of Alzheimer's disease. These are clusters that form in the spaces between the nerve cells.
Our brain is divided into various compartments assigned with different jobs to perform. The regions associated with memory are the amygdala, hippocampus, cerebellum, and the prefrontal cortex. When the functioning in any of these regions is disturbed, it causes memory-related problems.
One of such memory associated diseases is Alzheimer's disease. In India, more than 4 million people have some form of Alzheimer's. Worldwide, at least 44 million people are living with Alzheimer’s making this disease a global health crisis. As the population ages, the disease impacts a greater percentage of people.
1 in 3 of the seniors dies with Alzheimer's Disease or other dementia. In 2018, approximately INR 45,600 to INR 2,02,450 lifetime cost of care is required for a patient with AD. By 2050, it is predicted that the incidence of Alzheimer's will be detected every 33 seconds. Don't you think this situation will be dreadful?
Alzheimer's disease (AD), is a severe neurodegenerative disease. There are no initial symptoms of this disease. It starts to occur and eventually aggravates with time. In 60–70% of cases of AD, the person is not able to remember things and there is a gradual decrease in memory functions. The person faces difficulty in remembering recent events. This would be the start of AD.
As the disease progresses, there are problems related to language and speech, getting easily distracted with small disturbances (getting lost easily), mood swings, loss of motivation, not able to take care of oneself, behavioural issues, etc. The person starts getting detached from family and social life. Gradually, the body starts losing its functions, ultimately leading to death.
There are various mechanisms that are known to cause AD. One of which is the accumulation of 𝛃 amyloid proteins and tau proteins. The plaques are made up of beta-amyloid and tau, which is a protein peptide that has toxic effects on the function of the surrounding brain cells. Increase in production of these proteins leads to the forming of 𝛃 amyloid plaques and tau tangles, which leads to AD. Another link has been found out in a recent study that stated there is a gene that acts as a connecting link between the accumulated protein and AD.
This gene is called CAPON, that binds to the tau proteins. This gene is associated with the risk of various psychiatric related disorders. It is majorly found in one of the memory associated regions named hippocampus. It is revealed through studies that overexpression of this gene in the hippocampus regions, causes it to shrink. This shrinkage causes an increase in amyloid and tau proteins, which leads to AD.
The reverse is also true. If there is less of the CAPON gene, there are fewer tau proteins formed. Fewer tau proteins indicate less amyloid-β formation, that leads to less neurodegeneration. Thus, lesser brain shrivel. This regulation of on and off of genes becomes important in the treatments for AD. This study will give a new ray of hope to focus on the mechanisms of the CAPON gene activation.
A research work titled ‘Muscarinic and nicotinic acetylcholine receptor agonists: Current scenario in Alzheimer’s disease therapy’ was published in the year 2018 in the Journal of Pharmacy and Pharmacology (JPP) By Indian authors. These Indian authors were Ms Stuti Verma, Ms Ashwini Kumara, Mr Timir Tripathi and Mr Awanish Kumara. This study targets Muscarinic and Nicotinic type of acetylcholine receptor for the development of newer AD therapeutics.
Editor: Anomitra Dey
2. Shoko Hashimoto, Yukio Matsuba, Naoko Kamano, Naomi Mihira, Naruhiko Sahara, Jiro Takano, Shin-ichi Muramatsu, Takaomi C. Saido, Takashi Saito. Tau binding protein CAPON induces tau aggregation and neurodegeneration. Nature Communications, 2019; 10 (1) DOI: 10.1038/s41467-019-10278-x