Age‐related decline in neurogenesis: Old cells or old environment?

Zitnik, Galynn; Martin, George M.

doi:10.1002/jnr.10384

Cited by 36 publications

(22 citation statements)

References 45 publications

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“…These new neurons develop the morphological and functional properties of dentate granule cells and become integrated into existing neuronal circuitries (7,8). Although the function of hippocampal neurogenesis in adult is not yet clear, inhibition of hippocampal neurogenesis is associated with reduced learning and memory capacities (9), and impairment of hippocampal neurogenesis may be linked to cognitive decline in aging, Alzheimer's disease, and major depression (23)(24)(25). The factors involved in the regulation of hippocampal neurogenesis in adults are not well defined, but hormones, neurotransmitters, environmental stimuli, and growth factors have been identified as mediators (26).…”

Section: Discussionmentioning

confidence: 99%

Hypoglycemia Induces Transient Neurogenesis and Subsequent Progenitor Cell Loss in the Rat Hippocampus

et al. 2005

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Neurogenesis after brain injury not only leads to the replacement of damaged cells but might also contribute to functional recovery, suggesting the possibility of endogenous neural repair. We investigated the extent of hippocampal neural regeneration in a rat model of hypoglycemia. Two weeks after 30 min of insulin-induced isoelectric electroencephalogram, extensive neuronal loss was observed in the hippocampus, including area CA1 and dentate gyrus (DG). A transient increase in progenitor cell proliferation in the DG subgranular zone (SGZ) was detected, leading to an increase of immature neuroblasts 1-2 weeks after hypoglycemic insult. Most of the surviving newborn cells assumed a neuronal phenotype within 1 month in DG, a few cells near the site of granule-cell death becoming astroglia or microglia. No neuronal regeneration was observed in the CA1 after hypoglycemia, although dividing cells appeared to be astroglia or microglia in CA1 and dentate hilus. At 4 weeks after hypoglycemia, proliferative activity in the SGZ diminished below baseline in experimental versus control rats, with a subsequent reduction of neuroblasts. Morphological findings (doublecortin staining) suggest permanent progenitor cell loss in some areas of SGZ. Reduced neurogenesis in DG and lack of neuronal regeneration in CA1 may impede cognitive recovery after severe hypoglycemia injury.

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Section: Discussionmentioning

confidence: 99%

Hypoglycemia Induces Transient Neurogenesis and Subsequent Progenitor Cell Loss in the Rat Hippocampus

et al. 2005

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“…106 Indeed, recent studies have shown that neurogenesis is altered in a number neurodegenerative diseases, including Alzheimer's, 107,108 Huntington's, 109 and also with ageing 110 and epilepsy. 111 What follows is a discussion of the manner in which neurogenesis is altered in each of these pathological states, and the treatments that…”

Section: Regulators Of Neurogenesis In the Diseased Adult Brainmentioning

confidence: 99%

Regulators of Adult Neurogenesis in the Healthy and Diseased Brain

Grote

Hannan

2007

Clin Exp Pharma Physio

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SUMMARY1. In recent decades evidence has accumulated demonstrating the birth and functional integration of new neurons in specific regions of the adult mammalian brain, including the dentate gyrus of the hippocampus and the subventricular zone.2. Studies in a variety of models have revealed genetic, environmental and pharmacological factors that regulate adult neurogenesis. The present review examines some of the molecular and cellular mechanisms that could be mediating these regulatory effects in both the normal and dysfunctional brain.3. The dysregulation of adult neurogenesis may contribute to the pathogenesis of neurodegenerative disorders, such as Huntington's, Alzheimer's and Parkinson's disease, as well as psychiatric disorders such as depresssion. Recent evidence supports this idea and, furthermore, also indicates that factors promoting neurogenesis can modify the onset and progression of specific brain disorders, including Huntington's disease and depression.

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“…(3) In the cerebellum, the matrix cells of the rhombic lip are detached from the ventricular surface, migrate subpially to the external cerebellar surface, spread there as external matrix cells and give birth to internal granule neurons for sometime after birth (Fujita et al, 1966, Fujita, 1967a. These postnatal neurogeneses in the hippocampus and cerebellum, however, are reduced as the animals grow older (Zitnik and Martin, 2002). On the other hand, as a continuation of postnatal neuron production, some of the matrix cells persist longer than the physiological neuronogenesis, as long-persistent or remnant "neural stem cells", among nestin-positive ependymal cells Adapted from Fujita et al, 1985Fujita et al, , 1986.…”

Section: Regional Differences Of Matrix Cell Differentiation In the Cnsmentioning

confidence: 99%

The Discovery of the Matrix Cell, the Identification of the Multipotent Neural Stem Cell and the Development of the Central Nervous System

Fujita

2003

Cell Struct. Funct.

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ABSTRACT. In the early 1960s I applied 3 H-thymidine autoradiography to the study of the cells constituting the neural tube, and found that its wall was composed solely of one kind of single-layered epithelial cell, which perform an elevator movement between the mitotic and DNA-synthetic zones in the wall in accord with the cell cycle. They were identified as multipotent stem cells of the central nervous sytem (CNS) to which I gave the name of matrix cells.3 H-thymidine autoradiography also revealed the chronology of development of these matrix cells: At first they proliferate only to expand the population (stage I), then switch to differentiate specific neuroblasts in given sequences (stage II), and finally change themselves into ependymoglioblasts, common progenitors of ependymal cells and neuroglia (stage III). Based on these findings, I proposed a monophyletic view of cytogenesis of the central nervous sytem. This matrix cell theory claiming the existence of multipotent stem cells has long been the target of severe criticism and not been accepted among neuro-embryologists for a long time. Recent findings by experimental and clinical neuroscientists on the importance of stem cells have renewed interest in the nature and biology of the multipotent neural stem cells. The present paper describes how the concept of the matrix cell (multipotent neural stem cells in vivo) emerged and what has come out from this view over the last 45 years, and how the basic concept of the matrix cell theory has recently been reconfirmed after a long period of controversy and neglect.

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Age‐related decline in neurogenesis: Old cells or old environment?

Cited by 36 publications

References 45 publications

Hypoglycemia Induces Transient Neurogenesis and Subsequent Progenitor Cell Loss in the Rat Hippocampus

Hypoglycemia Induces Transient Neurogenesis and Subsequent Progenitor Cell Loss in the Rat Hippocampus

Regulators of Adult Neurogenesis in the Healthy and Diseased Brain

The Discovery of the Matrix Cell, the Identification of the Multipotent Neural Stem Cell and the Development of the Central Nervous System

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