Post-Stroke Environmental Enrichment Improves Neurogenesis and Cognitive Function and Reduces the Generation of Aberrant Neurons in the Mouse Hippocampus.

Ischemic lesions stimulate adult neurogenesis in the dentate gyrus, however, this is not associated with better cognitive function. Furthermore, increased neurogenesis is associated with the formation of aberrant neurons. In a previous study, we showed that a running task after a stroke not only increases neurogenesis but also the number of aberrant neurons without improving general performance.

Optimized Protocol for Proportionate CNS Cell Retrieval as a Versatile Platform for Cellular and Molecular Phenomapping in Aging and Neurodegeneration.

Efficient purification of viable neural cells from the mature CNS has been historically challenging due to the heterogeneity of the inherent cell populations. Moreover, changes in cellular interconnections, membrane lipid and cholesterol compositions, compartment-specific biophysical properties, and intercellular space constituents demand technical adjustments for cell isolation at different stages of maturation and aging. Though such obstacles are addressed and partially overcome for embryonic premature and mature CNS tissues, procedural adaptations to an aged, progeroid, and degenerative CNS environment are underrepresented.

Microglia-mediated phagocytosis of apoptotic nuclei is impaired in the adult murine hippocampus after stroke.

Following stroke, neuronal death takes place both in the infarct region and in brain areas distal to the lesion site including the hippocampus. The hippocampus is critically involved in learning and memory processes and continuously generates new neurons. Dysregulation of adult neurogenesis may be associated with cognitive decline after a stroke lesion.

Early Stroke Induces Long-Term Impairment of Adult Neurogenesis Accompanied by Hippocampal-Mediated Cognitive Decline.

Stroke increases neurogenesis in the adult dentate gyrus in the short term, however, long-term effects at the cellular and functional level are poorly understood. Here we evaluated the impact of an early stroke lesion on neurogenesis and cognitive function of the aging brain. We hypothesized that a stroke disturbs dentate neurogenesis during aging correlate with impaired flexible learning.

Cell-replacement therapy and neural repair in the retina.

Visual impairment severely affects the quality of life of patients and their families and is also associated with a deep economic impact. The most common pathologies responsible for visual impairment and legally defined blindness in developed countries include age-related macular degeneration, glaucoma and diabetic retinopathy. These conditions share common pathophysiological features: dysfunction and loss of retinal neurons.

Neurogenic potential of stem/progenitor-like cells in the adult mammalian eye.

The neural retina as part of the brain has received a great deal of attention since quiescent neural stem cells/progenitor cells (NSC/PCs) were discovered in this non-neurogenic region. Herein, we particularly feature the adult rodent eye and provide an overview of all putative neuronal progenitor-like cells attributed to the various ocular areas that have been identified during the last decade. These neuronal progenitor-like cells include the pigmented cells of the ciliary body (CB), as well as the pigmented cells of the iris and the retinal pigment epithelium (RPE).

In situ dividing and phagocytosing retinal microglia express nestin, vimentin, and NG2 in vivo.

Background: Following injury, microglia become activated with subsets expressing nestin as well as other neural markers. Moreover, cerebral microglia can give rise to neurons in vitro. In a previous study, we analysed the proliferation potential and nestin re-expression of retinal macroglial cells such as astrocytes and Müller cells after optic nerve (ON) lesion.

Simvastatin improves retinal ganglion cell survival and spatial vision after acute retinal ischemia/reperfusion in mice.

Purpose: The major aims of this study were to evaluate the effect of retinal ischemia by behavioral testing and histologic analyses, to visualize ischemia-induced changes of cortical activity by optical imaging of intrinsic signals, and to test the therapeutic effectiveness of simvastatin.

Methods: Retinal ischemia was induced monocularly by elevating intraocular pressure. Visual function was tested behaviorally with a virtual reality optomotor system, physiologically with optical imaging of intrinsic signals, and histologically by counting the surviving retinal ganglion cells (RGCs) in the same animal.

Proliferative response of microglia and macrophages in the adult mouse eye after optic nerve lesion.

Purpose: The purpose of this in vivo study was to evaluate the proliferative response of immunologic cells during the acute phase after optic nerve (ON) lesion in the neural retina and the ciliary body (CB) in the adult mouse.

Methods: The number of cells obtained 5 to 10 days after ON crush was compared with that counted after intraorbital ON transection. In addition, after ON crush, the time course of in situ proliferating Ki67(+) microglia and macrophages was analyzed from 6 hours up to 10 days.

Optic nerve lesion increases cell proliferation and nestin expression in the adult mouse eye in vivo.

In the naïve adult rodent eye cell proliferation does not occur. The aim of this in vivo study was to evaluate if quiescent putative progenitor-like cells within the adult mouse eye can be activated by optic nerve (ON) injury. For a comprehensive analysis, three areas were assessed: the ON, the neural retina, and the ciliary body (CB).