Cerebral Ischemia and Neurogenesis: A Two-time Comparison

Acute injuries to CNS such as stroke induce neural progenitor proliferation in adult brain which might be an endogenous attempt to self-repair. This process is known to be altered by several exogenous and endogenous modulators including growth factors that could help to reinforce the post-stroke neurogenesis. Increasing the neurogenesis may be a future therapeutic option to decrease the cognitive and behavioral deficits following stroke. In addition, transplantation of various types of stem cells into the injured brain is currently thought to be an exciting option to replace the neurons lost in the post-ischemic brain. These include immortalized stem cell lines, neural progenitors prepared from embryonic and adult animals and mesenchymal stem cells. Using exogenous stem cells in addition to modulating endogenous neurogenesis, we may be able to repair the injured brain after a devastating stroke. This article reviewed the current literature of these two issues.

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The potential of neural stem cells to repair stroke-induced brain damage

Liu

Lang

Başkaya

et al. 2009

Acta Neuropathol

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The Role of Autophagy in the Correlation Between Neuron Damage and Cognitive Impairment in Rat Chronic Cerebral Hypoperfusion

Zou

Song

et al. 2017

Mol Neurobiol

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Pathological changes and cognitive impairment caused by chronic cerebral hypoperfusion (CCH) have been previously reported. However, how these changes progress remains unclear. Additionally, there are few studies regarding the mechanism underlying the involvement of autophagy in these processes. Two-step bilateral common carotid artery occlusion (BCCAO) was performed to replicate CCH in Sprague Dawley rats. The animals were divided into seven groups, including a sham group and 2-, 4-, 8-, 12-, 16-, and 20-week BCCAO groups (n = 7 per group). Five additional rats were used to monitor cerebral blood fluid (CBF) changes via laser speckle contrast imaging (LSCI). We tested for cognitive changes and pathological changes, including neuronal injury, white matter lesions, and β-Amyloid (Aβ) deposition, via acknowledged methods. Autophagy was analyzed via western blotting and immunohistochemistry. Cognitive impairment appeared beginning at 8 weeks after BCCAO despite improvement in CBF. Neuronal damage began at 8 weeks in the hippocampal CA1 region and at 4 weeks in the cortex. White matter injury was detected in all BCCAO groups. Intracellular Aβ accumulation occurred earlier than extracellular plaque formation. The levels of autophagy-related proteins (Beclin-1, light chain 3B, and P62) increased beginning at 2 weeks in the cortex and at 4 weeks in the hippocampus and remained elevated throughout the remainder of the study period. Despite recovery of CBF, autophagy dysfunction occurred early after CCH and played an important role in neuronal deterioration, cognitive decline, and intracellular Aβ aggregation.

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The Cannabinoid Receptor Agonist WIN55,212-2 Ameliorates Hippocampal Neuronal Damage After Chronic Cerebral Hypoperfusion Possibly Through Inhibiting Oxidative Stress and ASK1-p38 Signaling

Wang¹,

Lin

et al. 2019

Neurotox Res

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Cerebral Ischemia and Neurogenesis: A Two-time Comparison

Cited by 6 publications

References 41 publications

The potential of neural stem cells to repair stroke-induced brain damage

The potential of neural stem cells to repair stroke-induced brain damage

The Role of Autophagy in the Correlation Between Neuron Damage and Cognitive Impairment in Rat Chronic Cerebral Hypoperfusion

The Cannabinoid Receptor Agonist WIN55,212-2 Ameliorates Hippocampal Neuronal Damage After Chronic Cerebral Hypoperfusion Possibly Through Inhibiting Oxidative Stress and ASK1-p38 Signaling

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