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. 2012 Jul 17:3:138.
doi: 10.3389/fphar.2012.00138. eCollection 2012.

Alzheimer's disease, neuroprotection, and CNS immunosenescence

Affiliations

Alzheimer's disease, neuroprotection, and CNS immunosenescence

Wolfgang J Streit et al. Front Pharmacol. .

Abstract

This review is focused on discussing in some detail possible neuroprotective functions of microglial cells. We strive to explain how loss of these essential microglial functions might contribute toward the development of characteristic neuropathological features that characterize Alzheimer's disease. The conceptual framework guiding our thinking is provided by the hypothesis that microglial senescence accounts for impaired neuronal protection and consequent neurodegeneration.

Keywords: Alzheimer’s disease; CNS immunosenescence; impaired neuronal protection; microglial cells; microglial senescence; neurodegeneration; neuropathological features; neuroprotection.

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Figures

Figure 1
Figure 1
Lectin staining of microglia (brown) in the normal cerebral cortex of a rabbit shows two microglial cells (arrows) extending their processes around cortical neurons. This close spatial relationship suggests ongoing interactions between resting microglia and neurons. Neurons are stained with cresyl violet. Scale bar: 50 μm.
Figure 2
Figure 2
Double immunofluorescent staining for microglia (Iba1) and Aβ protein (10D5) in the cerebral cortex of a human with Down syndrome reveals apparently normal, non-activated microglia in and around Aβ deposits. Microglia are ramified and show no evidence of having internalized any Aβ protein. Two microglial cells show presence of intracellular, autofluorescent lipofuscin (arrows). Scale bar: 50 μm.
Figure 3
Figure 3
Comparison of normal (ramified) and degenerating (dystrophic) microglia using Iba1 immunostaining in human cerebral cortex. (A) 22-year-old male non-demented subject reveals cells with normal morphology; (B) 48-year-old female subject with Down syndrome shows cells displaying obvious cytoplasmic fragmentation. Scale bar: 50 μm.

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References

    1. Anthony I. C., Bell J. E. (2008). The neuropathology of HIV/AIDS. Int. Rev. Psychiatry 20, 15–2410.1080/09540260701862037 - DOI - PubMed
    1. Araujo D. M., Cotman C. W. (1992). Beta-amyloid stimulates glial cells in vitro to produce growth factors that accumulate in senile plaques in Alzheimer’s disease. Brain Res. 569, 141–14510.1016/0006-8993(92)90380-R - DOI - PubMed
    1. Batchelor P. E., Liberatore G. T., Wong J. Y., Porritt M. J., Frerichs F., Donnan G. A., Howells D. W. (1999). Activated macrophages and microglia induce dopaminergic sprouting in the injured striatum and express brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor. J. Neurosci. 19, 1708–1716 - PMC - PubMed
    1. Berg D., Gerlach M., Youdim M. B., Double K. L., Zecca L., Riederer P., Becker G. (2001). Brain iron pathways and their relevance to Parkinson’s disease. J. Neurochem. 79, 225–23610.1046/j.1471-4159.2001.00608.x - DOI - PubMed
    1. Bessis A., Bechade C., Bernard D., Roumier A. (2007). Microglial control of neuronal death and synaptic properties. Glia 55, 233–23810.1002/glia.20459 - DOI - PubMed

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