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Angiogenesis, neurogenesis and brain recovery of function following injury.

ABSTRACT: Stroke and traumatic brain injury (TBI) are major causes of mortality and morbidity worldwide. Unfortunately, almost all phase III clinical trials of neuroprotective agents for stroke and TBI have demonstrated no benefit, raising concerns regarding the use of neuroprotective strategies alone as therapy for acute brain injuries. Therefore, a compelling need exists to develop treatments that promote both the repair and regeneration of injured brain tissue, and functional recovery. Recent data suggest that strategies to enhance neurogenesis and angiogenesis following brain injuries may provide promising opportunities to improve clinical outcomes and brain functional recovery. This review discusses neurogenesis and angiogenesis in the adult brain following stroke or TBI. Selected cell-based and pharmacological therapies are highlighted that promote neurogenesis and angiogenesis and are designed to restore neurological function after brain injuries. These discoveries emphasize the need for an improved understanding of injury- and therapy-induced neurogenesis and angiogenesis in the adult brain, and suggest that the manipulation of endogenous neural precursors and endothelial cells is a potential therapy for brain injury.

SUBMITTER: Xiong Y

PROVIDER: S-EPMC2836170 | biostudies-literature | 2010 Mar

REPOSITORIES: biostudies-literature

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Angiogenesis, neurogenesis and brain recovery of function following injury.

Xiong Ye Y Mahmood Asim A Chopp Michael M

Current opinion in investigational drugs (London, England : 2000) 20100301 3

Stroke and traumatic brain injury (TBI) are major causes of mortality and morbidity worldwide. Unfortunately, almost all phase III clinical trials of neuroprotective agents for stroke and TBI have demonstrated no benefit, raising concerns regarding the use of neuroprotective strategies alone as therapy for acute brain injuries. Therefore, a compelling need exists to develop treatments that promote both the repair and regeneration of injured brain tissue, and functional recovery. Recent data sugg ...[more]

PMID: 20178043

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Project description:In the adult mammalian brain, new neurons continue to be produced throughout life in two main regions in the brain, the subgranular zone (SGZ) in the hippocampus and the subventricular zone in the walls of the lateral ventricles. Neural stem cells (NSCs) proliferate in these niches, and migrate as neuroblasts, to further differentiate in locations where new neurons are needed, either in normal or pathological conditions. However, the endogenous attempt of brain repair is not very efficient. Calpains are proteases known to be involved in neuronal damage and in cell proliferation, migration and differentiation of several cell types, though their effects on neurogenesis are not well known. Previous work by our group has shown that the absence of calpastatin (CAST), the endogenous inhibitor of calpains, impairs early stages of neurogenesis. Since the hippocampus is highly associated with learning and memory, we aimed to evaluate whether calpain inhibition would help improve cognitive recovery after lesion and efficiency of post-injury neurogenesis in this region. For that purpose, we used the kainic acid (KA) model of seizure-induced hippocampal lesion and mice overexpressing CAST. Selected cognitive tests were performed on the 3rd and 8th week after KA-induced lesion, and cell proliferation, migration and differentiation in the dentate gyrus (DG) of the hippocampus of adult mice were analyzed using specific markers. Cognitive recovery was evaluated by testing the animals for recognition, spatial and associative learning and memory. Cognitive function was preserved by CAST overexpression following seizures, while modulation of post-injury neurogenesis was similar to wild type (WT) mice. Calpain inhibition could still be potentially able to prevent the impairment in the formation of new neurons, given that the levels of calpain activity could be reduced under a certain threshold and other harmful effects from the pathological environment could also be controlled.

Dataset Information

Angiogenesis, neurogenesis and brain recovery of function following injury.

Publications

Angiogenesis, neurogenesis and brain recovery of function following injury.

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