Welcome to Dr. Larisa Poluektova's Laboratory
Humanized mice for neuroAIDS
PI: L Poluektova
Source: NIH/NINDS 5 R21 NS060642-02
The specificity of HIV-1 for human cells precludes virus infection in most mammalian species and limits the use of small animal models for the studies of HIV-1 neuropathogenesis. We will investigate the establishment of a human cell network in the brain of NOD/scid-gc-/- mice transplanted with human CD34+ hematopoietic stem cells, their susceptibility to HIV-1, the mechanisms involved in the control of HIV-1 replication and neuronal damage. This model will be the best suited for NeuroAIDS research.
Neural Immunity in HIV Dementia
PI: H Gendelman; Project 3 Co-Leader: L Poluektova
Source: NIH/NINDS 5 P01 NS043985-07
The major goal of this grant is the study of the specific immunologic basis of HAD and linkages between it and other neurodegenerative disorders. This grant brings together in one organizational structure a group of scientists with expertise in areas of neurotoxicology, cellular immunology, neuropathology, neurophysiology, neuropharmacology and molecular biology, who maintain a unified focus on how MP biology affects both neurodegeneration and neuroprotection.
In Vivo Reconstitution Models for NeuroAIDS and Beta-Amyloidosis
PI: T Ikezu; Co-I: L Poluektova
Souce: NIH/NIMH 1 R01 MH083523-01
This study is focused on development of NeuroAIDS and beta-amyloidosis using severely compromised immunodeficient APP transgenic mice reconstituted with HIV-1-infected human immune cells.
Nanodelivery of Active NRTI to the Central Nervous System: Humanized HIV Murine Model
PI: S Vinogradov; Co-I: L Poluektova
Source: NIH/NINDS 1 R21 NS063879-01A1
Nanomedicine and NeuroAIDS
PI: H Gendelman; Co-I: L Poluektova
Source: NIH/NINDS 5 R01 NS36126-13
This research proposes to investigate the biophysiological properties of monocytes and monocyte-derived macrophages that influence cell migration both across the blood-brain barrier and within the brain. The central hypothesis is that changes in ion channel expression in monocytes and macrophages following exposure to virus and immune products influences the cell's ability to change its volume and shape, thus influencing cell migration. Such events are pivotal for macrophages to enter the brain and to secrete the toxins that underlie the neuropathogenesis of HIV-1 associated dementia.
Blood Brain Barrier Immune Compromise in NeuroAIDS
PI: G Kanmogne; Co-I: L Poluektova
Source: NIH/NIMH 5 R01 MH081780-02
The major goal of this project is to provide insights into the mechanisms by which cytokines and HIV-1 transduce signals at the blood-brain barrier (BBB), dysregulations that occurs in HIV infection and lead to BBB dysfunction.
In Memory - Jennifer Finke-Dwyer (October 19, 1978 - June 21, 2009), Research Technician II