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The Role of CD4+ T-Cell Senescence in Neurodegenerative Diseases:

As we age, our immune system changes, leading to the accumulation of senescent T-cells. These cells can cause chronic inflammation, known as "inflammaging," contributing to the decline in immune function and increasing vulnerability to neurodegenerative diseases like Alzheimer's, Parkinson's, and Multiple Sclerosis. Here's a deeper look into the mechanisms:


CD4+ T-Cells and Neurodegenerative Conditions:

  • Multiple Sclerosis (MS): Senescent CD4+ T-cells infiltrate the CNS, releasing proinflammatory cytokines (IFN-γ, TNF-α, IL-17) that damage myelin and neurons, exacerbating the disease.

  • Alzheimer's Disease (AD): T-cells in AD patients show signs of accelerated aging, including shortened telomeres and altered cytokine production, which correlate with disease severity.

  • Parkinson's Disease (PD): Inflammatory responses mediated by CD4+ T-cells contribute to neuronal damage and progression of PD.

Mechanistic Insights:

  • Metabolic Changes: Aging CD4+ T-cells exhibit increased glycolysis and mitochondrial dysfunction, leading to a proinflammatory state.

  • PI3K/Akt/mTOR Pathway: Key in T-cell senescence, with potential therapeutic interventions like rapamycin showing promise in rejuvenating immune function by modulating this pathway.

Therapeutic Strategies Targeting CD4+ T-cell senescence

  • Adoptive Transfer of Tregs: Enhancing regulatory T-cell function to suppress inflammation.

  • Monoclonal Antibodies: Targeting specific inflammatory pathways.

  • Metabolic Regulators: Using agents like metformin to alter T-cell metabolism and reduce inflammation.

Gao, Y., Lu, Y., Liang, X., Zhao, M., Yu, X., Fu, H., & Yang, W. (2024). CD4+ T-Cell Senescence in Neurodegenerative Disease: Pathogenesis and Potential Therapeutic Targets. Cells, 13(749)


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