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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Curr HIV Res. 2015;13(1):43–54. doi: 10.2174/1570162x13666150311164201

Fig. (1). Role of Tat and other HIV-1 proteins in neurodegeneration and treatment of HAND.

Fig. (1)

[A] Schematic representation of the mechanisms through which Tat might abnormally activate CDK5 in HAND. Tat could activate calpain 1, which in turn cleaves p35 to p25, this later fragment hyperactivates CDK5 leading to abnormal phosphorylation of Tau, CRMP2 and DCX and neurodegeneration. Alternatively, Tat could interact with p27, which is necessary to carry CDK5 to the nucleus. When Tat interferes with this role of p27, CDK5 is retained in the cytoplasm resulting in hyperactivation of CDK5 and neurodegeneration. (B) Potential targets for HAND therapeutics including blocking Tat, CDK5, p25 and pTau.