Synaptodendritic recovery following HIV Tat exposure: Neurorestoration by phytoestrogens.

Bertrand, Sarah J.; Mactutus, Charles F.; Aksenova, Marina V.; Espensen‐Sturges, Tori D.; Booze, Rosemarie M.

HIV-1 infects the brain and, despite antiretroviral therapy, many infected individuals suffer from HIV-1-associated neurocognitive disorders ( HAND). HAND is associated with dendritic simplification and synaptic loss. Prevention of synaptodendritic damage may ameliorate or forestall neurocognitive decline in latent HIV-1 infections. The HIV-1 transactivating protein (Tat) is produced during viral latency in the brain and may cause synaptodendritic damage. This study examined the integrity of the dendritic network after exposure to HIV-1 Tat by labeling filamentous actin (F-actin)-rich structures (puncta) in primary neuronal cultures. After 24 h of treatment, HIV-1 Tat was associated with the dendritic arbor and produced a significant reduction of F-actin-labeled dendritic puncta as well as loss of dendrites. Pre-treatment with either of two plant-derived phytoestrogen compounds (daidzein and liquiritigenin), significantly reduced synaptodendritic damage following HIV-1 Tat treatment. In addition, 6 days after HIV-1 Tat treatment, treatment with either daidzein, or liquiritigenin enhanced recovery, via the estrogen receptor, from HIV-1 Tat-induced synaptodendritic damage. These results suggest that either liquiritigenin or daidzein may not only attenuate acute synaptodendritic injury in HIV-1 but may also promote recovery from synaptodendritic damage.

HIV infections; PHYTOESTROGENS; ANTIRETROVIRAL agents; COGNITION disorders; FLAVANONES; CELL culture; F-actin; LABORATORY rats

Journal of Neurochemistry, 2014, Vol 128, Issue 1, p140

0022-3042

Academic Journal

10.1111/jnc.12375