Biomedical subjects

Jessica R Conde

Publications and source records attributed to Jessica R Conde.

3 recordsLinked to original sources

PubMed2006

Microglia in the aging brain.

The aging brain is characterized by a demonstrable decrease in weight and volume, particularly after the age of 50. This atrophy, which affects both grey and white matter, is presumed to result from a loss of neurons and myelinated axons. Glial cells, on the other hand, appear to increase in the aging brain, which exhibits greater immunoreactivity with both astrocytic and microglial markers. This review is focused on the morphologic and phenotypic changes that occur in microglial cells with normal aging. Although there is a consistent aging-related upregulation of microglial activation markers in experimental animals and humans that could be interpreted as aging-related neuroinflammation, it is generally difficult to show a direct correlation between ostensible microglial activation and neurodegeneration. This raises questions about whether aging-related microglial activation indeed represents reactive gliosis in the conventional sense. As an alternative, we discuss the possibility that structural and phenotypic changes that occur in microglia are a direct reflection of the aging process on microglia. Thus, microglia cells themselves may be subject to cellular senescence in the sense that they no longer function efficiently. The concept of microglial senescence offers a novel perspective on aging-related neurodegeneration, namely that neurodegeneration could also occur secondary to microglial degeneration.

Aging↗

PubMed2005

Effect of aging on the microglial response to peripheral nerve injury.

Microglial morphology and immunophenotype have been studied extensively in aging-related neurodegenerative diseases, but to a lesser extent in the normally aged CNS, and little is known about how aging affects the ability of microglia to respond to neuronal injury. The goal of the current study was to determine if aging affects the ability of microglia to divide during the early response to facial nerve axotomy. In addition, we investigated the incidence of microglial cell death during later post-axotomy time points to determine if aging had an effect on microglial turnover. We employed DNA labeling with 3H-thymidine, TUNEL and lectin histochemistry after facial nerve axotomy in young (3 months), middle-aged (15 months), and old (30 months) Fisher344-Brown Norway hybrid rats. Proliferation of microglia in old rats remained significantly higher than in young rats 4 days after injury, suggesting that regulation of microglial proliferation changes with aging. There was no aging-related difference in microglial TUNEL staining at 7, 14 or 21 days post-axotomy. Lectin histochemistry in the unoperated facial nucleus revealed aging-related morphological changes in resting microglia, including hypertrophy of the cytoplasm with dense perinuclear staining. Aging-related differences in activated microglia on the lesioned side were more subtle, although many activated microglia of aged animals continued to exhibit dense perinuclear lectin reactivity. We propose that aging-related changes in morphology in conjunction with a less regulated proliferative response in the aged facial nucleus may be a reflection of microglial senescence.

Aging↗

PubMed2005

Role of microglia in the central nervous system's immune response.

Microglial cells comprise a network of endogenous immunocompetent cells that pervade the brain and spinal cord. The primary function of this system is to provide continuous surveillance of the parenchyma and protect the central nervous system (CNS) during injury and disease. Here we discuss the involvement of microglia during brain aging and aging-related neurodegenerative disease, i.e. Alzheimer's disease, and briefly summarize their possible roles in amyotrophic lateral sclerosis (ALS). In addition, we provide an overview of the neuroinflammation associated with primary brain tumors and how microglial tumor cytotoxicity could be targeted for immunotherapeutic approaches designed to treat these lesions.

Alzheimer Disease↗