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Abstract

Background: Chronic Traumatic Encephalopathy (CTE) is a progressive neurodegenerative disorder associated with repetitive traumatic brain injury (TBI). Characterized by abnormal accumulation of hyperphosphorylated tau protein, CTE presents with a spectrum of cognitive, behavioral, and motor impairments. Understanding the role of tau protein in CTE is crucial for elucidating its pathogenesis and developing potential therapeutic interventions.

Objective: This review aims to examine the mechanisms by which tau protein contributes to neurodegeneration in CTE, focusing on the pathways leading to its accumulation and the subsequent neuronal damage observed in affected individuals.

Methods: We conducted a comprehensive review of current literature, including studies on tau pathology in CTE, animal models of repetitive brain injury, and clinical observations. Emphasis was placed on the molecular mechanisms underpinning tau hyperphosphorylation, its aggregation into neurofibrillary tangles, and the resulting neuronal dysfunction.

Results: Repetitive brain injury induces a cascade of pathological events leading to tau protein hyperphosphorylation. This post-translational modification disrupts tau’s normal role in stabilizing microtubules, resulting in tau aggregation and neurofibrillary tangles. The accumulation of these tangles contributes to synaptic loss, neuronal cell death, and the development of neuroinflammation. Additionally, recent findings suggest that tau pathology in CTE may exhibit distinct features compared to other tauopathies, potentially influencing disease progression and symptomatology.

Conclusion: Tau protein plays a pivotal role in the neurodegenerative processes observed in CTE. The understanding of tau-related mechanisms in CTE provides valuable insights into the broader implications of tauopathies and emphasizes the need for targeted therapies aimed at tau stabilization and reduction of tau aggregation. Future research should focus on identifying potential biomarkers for early diagnosis and developing therapeutic strategies to mitigate tau-related neurodegeneration in CTE.