Memory Deficit Accompanying Cerebral Neurodegeneration After Stroke in Stroke-Prone Spontaneously Hypertensive Rats (SHRSP)

Yamaguchi, Mai; Sugimachi, K; Nakano, Kaori; Fujimoto, Motoaki; Takahashi, Masaya; Chikugo, Takaaki; Ogawa, Hiroshi

doi:10.1007/978-3-7091-9334-1_54

Cited by 9 publications

(14 citation statements)

References 4 publications

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“…When compared to WKY rats, SHRSP rats had poor learning and memory during their pre stroke phase with worse outcomes post stroke [97]. SHRSP rats after stroke or when subjected to vessel occlusion models (such as UCCAO), with or without salt supplement demonstrate cognitive impairment and develop WM rarefaction and myelin damage, WM lesions with reactive gliosis, small vessel wall hardening, BBB disruption and inflammatory responses were observed [98–101].…”

Section: Comparison Of Three Multiple Infarction Vad Modelsmentioning

confidence: 99%

Models and mechanisms of vascular dementia

Venkat

Chopp

Chen

2015

Experimental Neurology

267

256

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Vascular Dementia (VaD) is the second leading form of dementia after Alzheimer’s disease (AD) plaguing the elderly population. VaD is a progressive disease caused by reduced blood flow to the brain, and it affects cognitive abilities especially executive functioning. VaD is poorly understood and lacks suitable animal models, which constrain the progress on understanding the basis of the disease and developing treatments. This review article discusses VaD, its risk factors, induced cognitive disability, various animal (rodent) models of VaD, pathology, and mechanisms of VaD and treatment options.

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Section: Comparison Of Three Multiple Infarction Vad Modelsmentioning

confidence: 99%

Models and mechanisms of vascular dementia

Venkat

Chopp

Chen

2015

Experimental Neurology

267

256

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“…Mice cannot tolerate sudden occlusion of both CCAs. Therefore, this model is only used in rats, including spontaneously hypertensive rats (Yamaguchi et al, 1994; Yamori et al, 1976). 2VO causes chronic cerebral hypoperfusion, especially in the forebrain, leading to early BBB disruption, WM rarefaction, axonal and myelin damage, hippocampal and cortical neuron damage, as well as neuroinflammation.…”

Section: Animal Models Of Vcidmentioning

confidence: 99%

The impact of cerebrovascular aging on vascular cognitive impairment and dementia

Yang

Sun

et al. 2017

Ageing Research Reviews

158

128

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As human life expectancy rises, the aged population will increase. Aging is accompanied by changes in tissue structure, often resulting in functional decline. For example, aging within blood vessels contributes to a decrease in blood flow to important organs, potentially leading to organ atrophy and loss of function. In the central nervous system, cerebral vascular aging can lead to loss of the integrity of the blood-brain barrier, eventually resulting in cognitive and sensorimotor decline. One of the major of types of cognitive dysfunction due to chronic cerebral hypoperfusion is vascular cognitive impairment and dementia (VCID). In spite of recent progress in clinical and experimental VCID research, our understanding of vascular contributions to the pathogenesis of VCID is still very limited. In this review, we summarize recent findings on VCID, with a focus on vascular age-related pathologies and their contribution to the development of this condition.

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“…The SHR represents a genetic model, and it is unknown whether neural and behavioral disturbances could be a parallel genetic phenomenon and not causally related to the elevated blood pressure per se. Nevertheless, it is interesting that deficits in cognitive processes have been also observed in stroke-prone SHR 34,42 and SHR developed by Koletsky (Golda and Petr 43 ). Because hypertension does not develop in the SHR until about 2 months of age, it would be interesting to compare the performance between young normotensive SHR and WKY.…”

Section: Nimodipine Reverses Cognitive Deficitsmentioning

confidence: 99%

Spontaneously Hypertensive Rats

Meneses

Hong

1998

Hypertension

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Abstract-Spontaneously hypertensive rats (SHR) of 3 to 12 months of age learned and retrieved less information than normotensive Wistar-Kyoto rats (WKY), although no difference was found with animals from 18 and 24 months of age. The combined influence of hypertension and aging had an additive detrimental effect on cognitive functions. Notwithstanding these deficiencies in learning and memory, SHR have seldom been used as a model in the screening of drugs with therapeutic potential for treatment of disorders of cognitive processes. Moreover, the calcium channel blocker nimodipine has beneficial effects on learning in both aged and hypertensive animals and humans. However, no attempt has been made to investigate whether nimodipine can reverse the additive deleterious effects of aging and hypertension in the same subject. We recently reported that deteriorated animals (middle-aged and/or hypertensive) chronically treated with nimodipine (via osmotic minipumps) exhibit higher learning scores. This information indicates that nimodipine can reverse the impairing effects of either aging or hypertension on learning; the presence of the two conditions, however, produces a severe impairment that can be partially reversed by this drug. Therefore, we propose that mature and middle-aged SHR represent a model for the screening of potentially useful drugs in the treatment of learning disorders, probably associated with hypertension and/or aging. Nevertheless, it must be remembered that the SHR is a genetic model and the appearance of neural disturbances could be a parallel genetic phenomenon and not necessarily or exclusively related to hypertension per se. (Hypertension. 1998;31:968-972.)Key Words: rats, inbred SHR Ⅲ learning Ⅲ memory Ⅲ aging Ⅲ pharmacology Ⅲ models A great expansion of experimental research began with the development of rat strains with genetically inherited hypertension. The SHR offers specific and uniform genetic predisposition, 1 thus allowing the study of the causes, mechanisms, and pathology of hypertension, as well as its behavioral consequences, and the comparison of the efficacy of proposed therapeutic interventions in relation to existing clinical treatments. Moreover, central neurohormonal mechanisms constitute the dominating trigger influence in SHR 1 and provide a model of hypertension that allows the study of the combined influence of both aging and hypertension on cognitive and physical functions on different developmental stages.2,3 Notwithstanding, the SHR is a genetic model, and the appearance of neural disturbances could be a parallel genetic phenomenon and not necessarily or exclusively related to the elevated blood pressure per se. Normal aging also produces a slow decline in neuron population, tissue distensibility, basal metabolic rate, and oxygen consumption, thus affecting cardiovascular performance. The aim of the present work was to present evidence obtained in our laboratory supporting the idea that the SHR is a suitable behavioral model to test drugs with potential therapeutic us...

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Memory Deficit Accompanying Cerebral Neurodegeneration After Stroke in Stroke-Prone Spontaneously Hypertensive Rats (SHRSP)

Cited by 9 publications

References 4 publications

Models and mechanisms of vascular dementia

Models and mechanisms of vascular dementia

The impact of cerebrovascular aging on vascular cognitive impairment and dementia

Spontaneously Hypertensive Rats

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