According to the Center for Disease Control and Prevention (CDC), Alzheimer's disease is "a progressive disorder beginning with mild memory loss possibly leading to loss of the ability to carry on a conversation and respond to the environment" (Alzheimer’s, 2015). It affects various crucial parts of the brain that control memory, thought, and language. The CDC further ads that the disease can affect an individual's ability to conduct daily activities. Despite the severity of the disease, scientists have struggled to understand the cause of Alzheimer's disease. According to statistics conducted by the CDC in 2014, almost 5 million Americans were living with the disease (Alzheimer’s, 2015). Although the precise cause of the disease remains unclear, research has promised to uncover the exact mechanism that allows the establishment of the disease in the brain. The concept behind the new study is based on a disruptive protein known as tau which accumulates preferentially in the excitatory neurons thus predisposing an individual to this disease.
Alzheimer's is primarily a neurodegenerative disorder, meaning that it involves the damaged and dying neurons. Also, important to note is that the disease is a growing epidemic, affecting approximately 50 million people worldwide (Alzheimer’s, 2015). Just like any other forms of dementia, the condition involves the accumulation of toxic substances in the form of proteins in the brain. The proteins in turn conglomerate to form plaques which in turn disrupt the cell to cell communication leading to cognitive problems in an individual. In many circumstances, the most assessed protein is known as the beta-amyloid known for its disruptive process in the brain. When pieces of this protein clump together, plaques are formed. Scientists have further opined that the beta-amyloid has sticky characteristics that assist it in the formation of plaques (Spires-Jones & Hyman, 2014). The clusters of the protein thereby block signaling between the cells at the synapses. Furthermore, the protein has also been suggested to activate the immune system cells thus triggering inflammation and damaging of the neurons.
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However, the newest study conducted in several institutions including the Columbia University Medical center in New York and Ohio State University in Columbus among others has built on a new protein known as tau that also accumulates on the brain cells. First, understanding the mechanism of the tau protein requires an appreciation of how a healthy brain works (Cohut, 2018). The neurons found in the brain have internal components referred to as the microtubules that not only support the cells but also contribute to their functions. The microtubules also function by carrying out vital substances from the interior to the outside of the cell where it connects to other components. In a healthy brain, the tau protein would normally bind and enhance stability on the microtubules. However, in Alzheimer's, tau behaves differently. Alterations in the brain chemistry cause the exit of the tau proteins from the microtubules and instead stick to one another (Chong et al., 2018). Eventually, the tau molecules that have been detached form long filaments that implicate the ability of the brain cells to communicate with one another.
The brain is made up of many cells with the most important ones being the neurons and the glial cells. The neurons play a vital role in communication and cognitive function while the glial cells function in protecting neurons. Furthermore, the neurons are classified into various types including the excitatory and the inhibitory. According to a research that utilized the brain of the mouse and that of individuals who had received a diagnosis for Alzheimer's, it was found out that the tau proteins had the most damaging impacts on the excitatory neurons which function to activate electrical impulses on the brain (Cohut, 2018). Questions have also been raised as to why the tau proteins preferentially target the excitatory cells. Genetic concepts involving a gene known as the BAG3 that codes for the clearance of tau in the brain have been used to explain this. The BAG3 expression is significantly higher in neuronal cells compared to others with high amounts seen in the inhibitory type. As such, this explains why the inhibitory cells have reduced susceptibility to the tau aggregates.
Therefore, the research on the disruptive tau muscles comes with great value especially with regards to the development of the disease's treatment. It remains critical to note that knowledge on why synapses degenerate during the disorder is an essential step towards the development of the treatment. The research conducted had made it apparent that the abnormal tau will be a vital target for inhibiting the formation of Alzheimer's. However, as earlier noted, the tau protein does not work alone. Any therapeutical intervention must also target the action of amyloid-beta protein which essentially acts by forming plaques that inhibit communication among the neurons. Therefore, a proper understanding of all the alterations that occur at the synapse level and the behavior of these proteins provide researchers with better ways of preventing the pathogenicity of the disease (Martin et al., 2013).
In conclusion, the concept behind the new research is based on a disruptive protein known as tau which accumulates preferentially in the excitatory neurons thus predisposing an individual to this disease. The new research adds to the existing one that revealed the actions of another disruptive protein known as the amyloid-beta. The tau protein primarily causes lengthy filaments on the excitatory neurons thereby inhibiting inter-cell communication. Therefore, this results in the degeneration of the brain cells causing the cognitive impairment that comes with the illness. Therefore, all therapeutic interventions must target the two proteins in a bid to prevent their toxicity on the neurons.
References
Alzheimer’s, A. (2015). 2015 Alzheimer's disease facts and figures. Alzheimer's & dementia: The journal of the Alzheimer's Association, 11(3), 332.
Chong, F. P., Ng, K. Y., Koh, R. Y., & Chye, S. M. (2018). Tau proteins and tauopathies in Alzheimer’s disease. Cellular and Molecular Neurobiology, 1-16.
Cohut, M. (2018). “Alzheimer's: Study zeroes in on brain's weakest link” Medical News Today https://www.medicalnewstoday.com/articles/324036.php
Martin, L., Latypova, X., Wilson, C. M., Magnaudeix, A., Perrin, M. L., Yardin, C., & Terro, F. (2013). Tau protein kinases: Involvement in Alzheimer's disease. Ageing Research Reviews, 12(1), 289-309.
Spires-Jones, T. L., & Hyman, B. T. (2014). The intersection of amyloid beta and tau at synapses in Alzheimer’s disease. Neuron, 82(4), 756-771.
