The National Institute of Neurological Disorders and Stroke (NINDS), the National Institute of Mental Health (NIMH), the National Institute on Drug Abuse (NIDA), and the National Institute on Aging (NIA) encourage grant applications for research on common immunological and inflammatory mechanisms involved in HIV-1 associated dementia (HAD) and neurodegenerative and/or autoimmune diseases of the nervous system such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS).
Immunologically mediated inflammatory processes are well-known to produce cellular damage in HIV infection and autoimmune diseases such as MS. In addition, there is growing—but still indirect—evidence that inflammatory processes may be involved in the pathogenesis of age-related neurodegenerative disorders such as AD. Although it has been demonstrated that neuronal damage associated with injury or infection initiates apoptotic neuronal death, there is little data in human neurons to define the mechanisms that might be involved. Research is needed to determine the events producing neuronal cell death due to inflammation or infection that may be common to diverse neurodegenerative or autoimmune diseases as well as those that may be unique to HIV-1 infection.
Examples of potential research areas include studies on: common pathways for activation of phagocytes/microglia and astroglia in HAD, autoimmune, and neurodegenerative disorders; common glial responses to chemokines, cytokines, or other inflammatory agents that have been identified as occurring in HAD, MS, or AD; the role of chemokine receptors in the normal function of the brain; the role of glial cells in providing neural protection both in infection and in immune-mediated injury; identification of any common alterations in blood-brain barrier permeability found in HAD, MS, or AD; the interaction of HIV-1 with other infectious agents; possible common histopathological and histochemical changes in neurons, microglia, or astroglia that may be found in neurodegenerative disorders, MS, or HAD using material from brain, animal models, or tissue culture; the role of noninfectious environmental agents in modulating activation of macrophages/microglia and astroglia during the progression of HAD, MS, or AD; excitotoxicity or increased oxidative stress and their role in producing the apoptosis observed in HAD and AD; and susceptibility genes that may be common to individuals developing HAD, MS, or AD.
For more information, potential applicants should contact Dr. A.P. Kerza-Kwiatecki, Neural Environment Cluster, NINDS, Neuroscience Center, 6001 Executive Boulevard, Room 2115, Bethesda, MD 20892; telephone: (301) 496-1431; fax: (301) 402-2060; e-mail: firstname.lastname@example.org.