Microglia and neuroprotection: implications for Alzheimer's disease.
The first part of this paper summarizes some of the key observations from experimental work in animals that support a role of microglia as neuroprotective cells after acute neuronal injury. These studies point towards an important role of neuronal-microglial crosstalk in the facilitation of neuroprotection. Conceptually, injured neurons are thought to generate rescue signals that trigger microglial activation and, in turn, activated microglia produce trophic or other factors that help damaged neurons recover from injury. Against this background, the second part of this paper summarizes recent work from postmortem studies conducted in humans that have revealed the occurrence of senescent, or dystrophic, microglial cells in the aged and Alzheimer's disease brain. These findings suggest that microglial cells become increasingly dysfunctional with advancing age and that a loss of microglial cell function may involve a loss of neuroprotective properties that could contribute to the development of aging-related neurodegeneration.
Streit
Wolfgang J
WJ
Department of Neuroscience, University of Florida College of Medicine, Gainesville, 32610-0244, USA. streit@mbi.ufl.edu
D000375:Aging; D000544:Alzheimer Disease / Q000628:therapy; D000818:Animals; D001930:Brain Injuries / Q000150:complications / Q000628:therapy*; D004195:Disease Models, Animal; D006801:Humans; D017628:Microglia / Q000502:physiology*; D009410:Nerve Degeneration / Q000209:etiology / Q000517:prevention & control*; D009474:Neurons / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use*
D018696:Neuroprotective Agents