Chronic traumatic encephalopathy refers to a neurodegenerative disorder that is associated with recurrent head injuries. The condition is characterized by progressive degeneration of brain cells, impacting emotional and motor functioning. The condition does not occur immediately when the head traumas happen but is closely linked with persistent post-concussive symptoms and second impact syndrome. CTE mainly affects the frontal and temporal lobes, although it can also affect other brain regions. Researchers believe that the pathologic changes in CTE are due to the accumulation of a protein called tau, which can interfere with neuronal signaling and lead to cell death. However, the development of tau proteins in CTE differs from those that develop during the development of Alzheimer’s disease.
Tau, in other terms, the microtubule-associated protein tau, is crucial in facilitating the normal translocation of cellular cargo within the neuronal axonal projections (Katsumoto et al., 2019). In its normal state, tau is a soluble protein and plays a crucial role in microtubule stabilization in cells. The highest concentrations of the particular protein are found in the neurons. However, in pathology, tau is more phosphorylated than normal. Hyperphosphorylated tau molecules that detach from microtubules in the axon and move to the cell body and proximal dendrites affect the axonal function and form Neurofibrillary tangles (NFTs). Tau protein accumulates in neurons and other brain cells with time. The presence of particular proteins around blood vessels in the brain is the main way CTE is identified at the cellular level. Neurofibrillary tangles (NFTs), consisting of twisted tau protein strands, are a particular kind of tau that that keeps on accumulating over time and are closely linked to the development of CTE. NFTs are present in the soma and dendrites of neurons, astrocytes, microglia, and oligodendrocytes, among other types of cells. The buildup of tau in CTE impairs neurons’ ability to function normally, which causes a deterioration in cognitive, emotional, and motor abilities.
The widespread damage to the brain that characterizes CTE is the main issue that takes place at the tissue level. Major changes include the loss of neurons, gliosis (an abnormal accumulation of glial cells), and the development of NFT. Tau protein buildup is thought to cause neuronal loss since it can obstruct neuronal signaling and result in cell death (Iverson et al., 2019). Another distinctive aspect of CTE is gliosis, an excessive buildup of glial cells thought to be a reaction to brain injury. One of the hallmarks of CTE is the development of NFTs in neurons and other cells associated with interference with cognitive, emotional, and motor functions.
Morphologic changes brought on by CTE may result in several functional issues. Neuronal death may have adverse repercussions such as memory loss, disorientation, and impaired judgment. Poor neuronal transmission brought on by gliosis may impair one’s capacity for abstract thought, language, and problem-solving. Neuronal signaling may be compromised due to the growth of NFTs, which may impair cognitive, emotional, and motor function (Mayo clinic, 2023). Additionally, a buildup of tau protein may prevent neurotransmitters from being released normally, lowering motivation and attentiveness.
In conclusion, tau protein builds up in neurons and other brain cells, causing CTE, a neurodegenerative illness that worsens with time. NFTs, which can disrupt neural signaling and cause a decrease in cognitive, affective, and motor performance, is a hallmark of CTE at the cellular level. Neuronal loss, gliosis, and the development of NFTs are tissue-level indicators of CTE, which can cause various functional abnormalities. It is critical to recognize and treat CTE as early as possible since the morphologic changes in CTE can result in a deterioration in cognitive, emotional, and motor functions.
References
Iverson, G. L., Gardner, A. J., Shultz, S. R., Solomon, G. S., McCrory, P., Zafonte, R., … & Castellani, R. J. (2019). Chronic traumatic encephalopathy neuropathology might not be inexorably progressive or unique to repetitive neurotrauma. Brain, 142(12), 3672–3693. https://academic.oup.com/brain/article-pdf/142/12/3672/31499403/awz286.pdf
Katsumoto, A., Takeuchi, H., & Tanaka, F. (2019). Tau pathology in chronic traumatic encephalopathy and Alzheimer’s disease: similarities and differences. Frontiers in neurology, pp. 10, 980. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6748163/
Mayo Clinic (2023). Chronic traumatic encephalopathy. https://www.mayoclinic.org/diseases-conditions/chronic-traumatic-encephalopathy/symptoms-causes/syc-20370921
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