Journal
JOURNAL OF NEUROIMMUNE PHARMACOLOGY
Volume 5, Issue 3, Pages 294-309Publisher
SPRINGER
DOI: 10.1007/s11481-010-9205-z
Keywords
HIV; HIV-associated neurocognitive disorder; intranasal delivery; chemokines; oxidative stress; excitotoxicity; adult neurogenesis; synaptic signaling; cell cycle
Categories
Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS041202, R01NS056885, R01NS043994, F31NS060635, F32NS067945] Funding Source: NIH RePORTER
- NINDS NIH HHS [F32 NS067945-01, F31 NS060635-02, R01 NS043994, F31 NS060635-03, R01 NS056885, R01 NS043994-08, R01 NS041202] Funding Source: Medline
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Human immunodeficiency virus type 1 (HIV) infection presently affects more that 40 million people worldwide, and is associated with central nervous system (CNS) disruption in at least 30% of infected individuals. The use of highly active antiretroviral therapy has lessened the incidence, but not the prevalence of mild impairment of higher cognitive and cortical functions (HIV-associated neurocognitive disorders) as well as substantially reduced a more severe form dementia (HIV-associated dementia). Furthermore, improving neurological outcomes will require novel, adjunctive therapies that are targeted towards mechanisms of HIV-induced neurodegeneration. Identifying such molecular and pharmacological targets requires an understanding of the events preceding irreversible neuronal damage in the CNS, such as actions of neurotoxins (HIV proteins and cellular factors), disruption of ion channel properties, synaptic damage, and loss of adult neurogenesis. By considering the specific mechanisms and consequences of HIV neuropathogenesis, unified approaches for neuroprotection will likely emerge using a tailored, combined, and non-invasive approach.
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