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Posted On: 03/08/2024 8:32:06 PM
Post# of 148878
CONCLUSION
There is ample evidence that the immune response is involved in the pathogenesis of AD; the neuroinflammation hypothesis is highly attractive and is a powerful complement to the Aβ and tau protein hypotheses. During neuroinflammation, Aβ deposition activates astrocytes and microglia, with the latter transforming from a protective to a proinflammatory phenotype. Acute inflammation at the early stage is beneficial for clearing Aβ and repairing neuronal damage. However, with the progression of AD, microglia and astrocytes secrete proinflammatory cytokines and chemokines, leading to excessive and uncontrolled inflammation and neuron death. The CCL5/CCR5 axis plays an important role in learning, memory, neuroinflammation, and AD pathogenesis; however, the mechanistic details of CCL5/CCR5 axis in AD have not been fully elucidated and some of the existing evidence is contradictory. Even population-based studies on the distribution of the CCR5Δ32 allele have shown no association between CCL5/CCR5 and AD development. A reason for these conflicting findings may be differences in animal models and populations, but it is also possible that CCR5 has as-yet unidentified functions in the CNS. More studies are needed to explore the specific role of the CCL5/CCR5 signaling axis in AD pathogenesis in order to determine whether it can serve as a therapeutic target in treatment of AD. In addition, we believe that it will also be a potentially valuable idea to expand the scope of exploring CCL5/CCR5 axis to other neurodegenerative diseases.
https://academic.oup.com/jnen/article/82/11/8...#421627530
There is ample evidence that the immune response is involved in the pathogenesis of AD; the neuroinflammation hypothesis is highly attractive and is a powerful complement to the Aβ and tau protein hypotheses. During neuroinflammation, Aβ deposition activates astrocytes and microglia, with the latter transforming from a protective to a proinflammatory phenotype. Acute inflammation at the early stage is beneficial for clearing Aβ and repairing neuronal damage. However, with the progression of AD, microglia and astrocytes secrete proinflammatory cytokines and chemokines, leading to excessive and uncontrolled inflammation and neuron death. The CCL5/CCR5 axis plays an important role in learning, memory, neuroinflammation, and AD pathogenesis; however, the mechanistic details of CCL5/CCR5 axis in AD have not been fully elucidated and some of the existing evidence is contradictory. Even population-based studies on the distribution of the CCR5Δ32 allele have shown no association between CCL5/CCR5 and AD development. A reason for these conflicting findings may be differences in animal models and populations, but it is also possible that CCR5 has as-yet unidentified functions in the CNS. More studies are needed to explore the specific role of the CCL5/CCR5 signaling axis in AD pathogenesis in order to determine whether it can serve as a therapeutic target in treatment of AD. In addition, we believe that it will also be a potentially valuable idea to expand the scope of exploring CCL5/CCR5 axis to other neurodegenerative diseases.
https://academic.oup.com/jnen/article/82/11/8...#421627530
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