Cognitive Improvement Induced by Environment Enrichment in Chronic Cerebral Hypoperfusion Rats: a Result of Upregulated Endogenous Neuroprotection?

Yang, Ying; Zhang, Junjian; Xiong, Li; Deng, Min; Wang, Jing; Xin, Jiawei; Liu, Hui

doi:10.1007/s12031-015-0529-2

Cited by 21 publications

(14 citation statements)

References 28 publications

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“…Chronic cerebral hypoperfusion (CCH) is a prevalent pathophysiological state in patients with Alzheimer's disease (AD) and vascular dementia (VaD). CCH has been identified as one of the initial conditions that are critical in the development of cognitive dysfunction [193].…”

Section: Chronic Hypoxia and Brain Responsementioning

confidence: 99%

Small Vessel Disease-Related Dementia: An Invalid Neurovascular Coupling?

Moretti

Caruso

2020

IJMS

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The arteriosclerosis-dependent alteration of brain perfusion is one of the major determinants in small vessel disease, since small vessels have a pivotal role in the brain’s autoregulation. Nevertheless, as far as we know, endothelium distress can potentiate the flow dysregulation and lead to subcortical vascular dementia that is related to small vessel disease (SVD), also being defined as subcortical vascular dementia (sVAD), as well as microglia activation, chronic hypoxia and hypoperfusion, vessel-tone dysregulation, altered astrocytes, and pericytes functioning blood-brain barrier disruption. The molecular basis of this pathology remains controversial. The apparent consequence (or a first event, too) is the macroscopic alteration of the neurovascular coupling. Here, we examined the possible mechanisms that lead a healthy aging process towards subcortical dementia. We remarked that SVD and white matter abnormalities related to age could be accelerated and potentiated by different vascular risk factors. Vascular function changes can be heavily influenced by genetic and epigenetic factors, which are, to the best of our knowledge, mostly unknown. Metabolic demands, active neurovascular coupling, correct glymphatic process, and adequate oxidative and inflammatory responses could be bulwarks in defense of the correct aging process; their impairments lead to a potentially catastrophic and non-reversible condition.

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Section: Chronic Hypoxia and Brain Responsementioning

confidence: 99%

Small Vessel Disease-Related Dementia: An Invalid Neurovascular Coupling?

Moretti

Caruso

2020

IJMS

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“…Oxidative stress has been strongly correlated to the pathogenesis of VaD (Liu and Zhang, ; Yang et al, ). Excess reactive oxygen and nitrogen species generated following excitotoxic insults induce significant changes in redox status associated with oxidative damage to cellular and vascular structures, in which protein oxidation, cleavage of DNA, and inhibition of the mitochondrial electron transport chain are the main features (Calabrese et al, ; Di Marco et al, ).…”

Section: Mitochondrial Dysfunction Inflammasomes and Neuroinflammatmentioning

confidence: 99%

Major pathogenic mechanisms in vascular dementia: Roles of cellular stress response and hormesis in neuroprotection

Calabrese

Giordano

Signorile

et al. 2016

J of Neuroscience Research

126

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Vascular dementia (VaD), considered the second most common cause of cognitive impairment after Alzheimer disease in the elderly, involves the impairment of memory and cognitive function as a consequence of cerebrovascular disease. Chronic cerebral hypoperfusion is a common pathophysiological condition frequently occurring in VaD. It is generally associated with neurovascular degeneration, in which neuronal damage and blood-brain barrier alterations coexist and evoke beta-amyloid-induced oxidative and nitrosative stress, mitochondrial dysfunction, and inflammasome- promoted neuroinflammation, which contribute to and exacerbate the course of disease. Vascular cognitive impairment comprises a heterogeneous group of cognitive disorders of various severity and types that share a presumed vascular etiology. The present study reviews major pathogenic factors involved in VaD, highlighting the relevance of cerebrocellular stress and hormetic responses to neurovascular insult, and addresses these mechanisms as potentially viable and valuable as foci of novel neuroprotective methods to mitigate or prevent VaD. © 2016 Wiley Periodicals, Inc.

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“…Although the mechanisms whereby EE preserves cognition remain obscure, numerous studies have suggested that the functional improvement related to EE is associated with the up-regulation of neurotrophic factors, the enhancement of synaptic plasticity, and the stimulation of neurogenesis [28], and the reduction of apoptosis and oxidative damage [29,30]. Learning and memory processes linked to differentiating PV interneuron networks can be regulated by recent experience, suggesting that EE may modulate cognition by targeting the differentiation state of PV neurons in the adult [31].…”

Section: Discussionmentioning

confidence: 99%