Differential susceptibility of senile and lesion-induced astrogliosis to phosphatidylserine

Jegliński, W; Pepeu, Giancarlo; Oderfeld-Nowak, B

doi:10.1016/s0197-4580(96)00209-6

Cited by 3 publications

(1 citation statement)

References 27 publications

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“…In the ␤-amyloid transgenic mouse, in which overexpression was controlled by a neuronal promoter, reactive gliosis accompanied extensive neurodegeneration and apoptosis as expected, but was also present in regions where minor neuronal changes were observed . Based on these studies, glial activation may be an early indicator of changes in neuronal-glial interactions during the process of aging and then eventually becomes either a sign of or a contributor to neurodegeneration and reactive gliosis (Jorgensen et al, 1993;Martin et al, 1994;Goss and Morgan, 1995;Jelinski et al, 1997).…”

Section: Reactive Gliosis and Glial Activationmentioning

confidence: 99%

Glial responses to steroids as markers of brain aging

Nichols

1999

J. Neurobiol.

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Glia mediate neuroendocrine and neuroimmune functions that are altered during the process of normal aging. The biological functions of glia are also important in synaptic remodeling and the loss of synaptic connections that occur during aging. These functions are carried out by changes in glia, including changes in shape, interactions with neurons and other glia, and gene expression. The predominant change that occurs in glia during aging is glial activation, which can progress to reactive gliosis in response to neurodegeneration. More markers are needed to distinguish normal and reactive glia. During aging, astrocytes hypertrophy and exhibit signs of metabolic activation, and astrocytic processes surround neurons. Microglia also become activated and subsets of activated microglial increase in number and may enter the phagocytic or reactive stage. Glial markers of brain aging and glial activation include glial fibrillary acidic protein (GFAP) and transforming growth factor (TGF)‐β1, which are increased in astrocytes and microglia, respectively. Steroids regulate the interactions between glia and neurons and glial gene expression, including GFAP and TGF‐β1. Therefore, changes in these parameters during aging may be due to altered steroid regulation. In general, the effects of steroids oppose the effects of aging. Recent data indicate that steroid treatment can decrease the expression of GFAP in the aged brain, yet GFAP is resistant to down‐regulation by endogenous glucocorticoids. Cellular and molecular markers of glial activation are being used to determine how changes in neuroendocrine and neuroimmune regulation contribute to repair and functional recovery that may reverse synaptic loss and cognitive impairment during aging. © 1999 John Wiley & Sons, Inc. J Neurobiol 40: 585–601, 1999

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Section: Reactive Gliosis and Glial Activationmentioning

confidence: 99%

Glial responses to steroids as markers of brain aging

Nichols

1999

J. Neurobiol.

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Astroglial heterogeneity closely reflects the neuronal-defined anatomy of the adult murine CNS

2006

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Astroglia comprise an extremely morphologically diverse cell type that have crucial roles in neural development and function. Nonetheless, distinct regions of the CNS have traditionally been defined by the phenotypic characteristics and connectivity of neuros. In a complementary fashion, we present evidence that discrete regions of the adult CNS can be delineated based solely on the morphology, density and proliferation rates of astroglia. We used transgenic hGFAP-GFP mice in which robust expression of GFP in adult astroglia enables detailed morphological characterization of this diversely heterogeneous cell population with 3D confocal microscopy. By using three complementary methods for labeling adult astroglia (hGFAP-GFP expression, and GFAP and S100beta immunostaining), we find that there is a remarkably diverse, regionally stereotypical array of astroglial morphology throughout the CNS, and that discrete anatomical regions can be defined solely on the morphology of astroglia within that region. Second, we find that the density of astroglia varies dramatically across the CNS, and that astroglial density effectively delineates even the sub-regions of complex structures, such as the thalamus. We also find that regional astroglial density varies depending on how astroglia are labeled. To quantify and illustrate these broad differences in astroglial density, we generated an anatomical density atlas of the CNS. Third, the proliferation rate, or mitotic index, of astroglia in the adult CNS also effectively defines anatomical regions. These differences are present regardless of the astroglial-labeling method used. To supplement our atlas of astroglial density we generated an atlas of proliferation density for the adult CNS. Together, these studies demonstrate that the morphology, density and proliferation rate of astroglia can independently define the discrete cytoarchitecture of the adult mammalian CNS, and support the concept that regional astroglial heterogeneity reflects important molecular and functional differences between distinct classes of astroglia, much like the long-accepted heterogeneity of neuronal populations.

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Mild cognitive impairment: animal models

Pepeu

2004

Dialogues in Clinical Neuroscience

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Mild cognitive impairment (MCI) is an aspect of cognitive aging that is considered to be a transitional state between normal aging and the dementia into which it may convert. Appropriate animal models are necessary in order to understand the pathogenic mechanisms of MCI and develop drugs for its treatment. In this review, we identify the features that should characterize an animal model of MCI, namely old age, subtle memory impairment, mild neuropathological changes, and changes in the cholinergic system, and the age at which these features can be detected in laboratory animals. These features should occur in aging animals with normal motor activity and feeding behavior. The animal models may be middle-aged rats and mice, rats with brain ischemia, transgenic mice overexpressing amyloid precursor protein and presenilin 1 (tested at an early stage), or aging monkeys. Memory deficits can be detected by selecting appropriately difficult behavioral tasks, and the deficits can be associated with neuropathological alterations. The reviewed literature demonstrates that, under certain conditions, these animal species can be considered to be MCI models, and that cognitive impairment in these models responds to drug treatment.

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Differential susceptibility of senile and lesion-induced astrogliosis to phosphatidylserine

Cited by 3 publications

References 27 publications

Glial responses to steroids as markers of brain aging

Glial responses to steroids as markers of brain aging

Astroglial heterogeneity closely reflects the neuronal-defined anatomy of the adult murine CNS

Mild cognitive impairment: animal models

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