Neurogenesis and Alzheimer’s Disease
There is a compensatory mechanism for replacing cells lost due to the degeneration seen in Alzheimer’s disease. Neurogenesis is seen in a lot of inflamed states of the brain such as trauma and stroke. Inflammation may lead to impaired hippocampal neurogenesis due to the extensive amyloid deposition causing the plaques and tangles. (Zhoa 2007) Alzheimer’s disease patients’ hippocampus had increased expression of neurogenesis markers and an increased number of cells expressing these markers. (Jin 2004) Beta amyloid protein impaired proliferation and neuronal differentiation of cultured human progenitor cells promoted apoptosis. Abnormalities in these progenitor cells may cause pathologies in learning and memory. Beta-amyloid deposition and the inflammatory response of microglia cause cognitive/behavior abnormalities seen in Alzheimer’s Disease. (Haughey 2002 and Zhoa 2007)
Neurogenesis and Parkinson’s Disease
Neurogenesis in the substantia nigra is a slower rate than hippocampus and olfactory bulb in Parkinson’s disease (Zhoa 2003). Constant glial replacement in the substantia nigra (SN) are key regulators of synaptic transmission and extracellular homeostasis. New cells all end up being glial and not differentiating into neurons (gliogenesis) for neurons need environmental signals. Implantation of stem cells into this region has been a therapy in the past. Implantation of SN progenitor cells expressed immature and mature markers after three weeks which also showed signs that they entered the hippocampal circuit, the sight of the most damage in Parkinson’s disease. (Lie 2002). Significant negative correlation between the number of of activated microglia and and the number of surviving hippocampal neurons (Ekdahl 2003).
Neurogenesis and Huntington’s Disease
In the Huntington’s diseased brain there is an increase of cell proliferation in the subependymal layer which is the site of damage. (Curtis 2005) Loss of GABAergic medium spiny projection neurons (special morphology of neuron) has shown increases subventricular zone progenitor cell proliferation and subsequent migration. The new cells extending from subventricular zone into damaged areas differentiate into cells that have neuronal morphologies and express NeuN (Tatterfield 2004). It is possible for endogenous progenitor cells to be utilized to replace cells lost through brain injury or disease, however this is untested in humans and not available yet.
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