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Transcript
Luis V. Colom, MD, PhD
VP of Research
Center for Biomedical Studies
Phone: 956-882-5048
Email: [email protected]
Current research interest:
Investigating the mechanisms underlying brain
dysfunction in Alzheimer’s disease.
Research:
Alzheimer’s disease (AD) is the 7th leading
cause of death in the United States, affecting
5.3 million people. The extracellular deposit of
amyloid beta peptides (Aβ), senile plaques in cerebral cortical regions, constitutes a hallmark lesion
of AD. In addition, diminished basal forebrain cholinergic and cortical glutamatergic functions
observed in AD cause most of the neuropsychological deficits in AD patients.
Current Studies:
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Aβ effects on septal neurons
Limited deposition of Aβ within the
hippocampus lesions axon terminals of septal
cholinergic and glutamatergic neurons.
Damaged hippocampal axon terminals lead to
altered somatic functions and subsequent
death of cholinergic and glutamatergic septal
neurons (injured cortical axons will lead to
neuronal death in additional basal forebrain
structures).
Altered properties of the surviving septal
neurons
Oxidative Stress
Our lab focuses on septohippocampal anatomical and functional alterations in Alzheimer’s disease
models.
The techniques applied to this research project are mRNA extraction,
Immunohistochemistry, stereology, confocal microscopy, Extracellular recordings and patch clamp
recordings.
Ongoing Research:



Anatomical studies of septal
cholinergic,
GABAergic
and
glutamatergic neurons
Theta rhythm dependent- synaptic
plasticity of the hippocampus
Brain processes that depend on
hippocampal synaptic plasticity,
such as certain learning and
memory processes.
Behavioral Studies:
Spatial memory tests using a Barnes
maze to observe alterations in
Alzheimer disease models.
Grant Support
NIH grant SC1NS065386 to Luis V. Colom