Dr. Poluektova's Lab

Welcome to Dr. Larisa Poluektova's Laboratory

Collaborators
Research Goals
Funding
Techniques used in the laboratory
Personnel 
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Collaborators:

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Research Goals:

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Funding:

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.

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Techniques used in the laboratory:

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Personnel:

Sidra_Akhter

Sidra Akhter
Research Technician

sidra.akhter@unmc.edu

 Tanuja_Gutti

Tanuj Gutti
Research Technologist

tgutti@unmc.edu

 

 

 Jaclyn_Knibbe

Jaclyn Knibbe
Research Technologist

jknibbe@unmc.edu

 

 

 Edward_Makarov

Edward Makarov
Research Technoligist

makarove@unmc.edu

In Memory - Jennifer Finke-Dwyer (October 19, 1978 - June 21, 2009), Research Technician II

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