scholarly journals Lipid Peroxidation in Chronic Cerebral HypoperfusionInduced Neurodegeneration in Rats

2020 ◽  
Vol 10 (2) ◽  
Author(s):  
Anil Kumar S ◽  
Saif SA ◽  
Oothuman P ◽  
Mustafa MIA
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lipid Peroxidation ◽  
Neurodegenerative Disorders ◽  
Neuronal Damage ◽  
Neuronal Cell ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Control Group ◽  
Vessel Occlusion

Introduction: Reduced cerebral blood fl ow is associated with neurodegenerative disorders and dementia, in particular. Experimental evidence has demonstrated the initiating role of chronic cerebral hypoperfusion in neuronal damage to the hippocampus, the cerebral cortex, the white matter areas and the visual system. Permanent, bilateral occlusion of the common carotid arteries of rats (two vessel occlusion - 2VO) has been introduced for the reproduction of chronic cerebral hypoperfusion as it occurs in Alzheimer’s disease and human aging. Increased generation of free radicals through lipid peroxidation can damage neuronal cell membrane. Markers of lipid peroxidation have been found to be elevated in brain tissues and body fl uids in neurodegenerative diseases, including Alzheimer’s disease, Parkinson disease and amyotrophic lateral sclerosis. Materials and Methods: Malondialdehyde (MDA), final product of lipid peroxidation, was estimated by thiobarbituric acid-reactive substances (TBARS) assay kit at eight weeks after induction of 2VO in the rats and control group. Results: Our study revealed a highly signifi cant (p<0.001) increase in the mean MDA concentration (12.296 ± 1.113 μM) in 2VO rats as compared to the control group (5.286 ± 0.363 μM) rats. Conclusion: Therapeutic strategies to modulate lipid peroxidation early throughout the course of the disease may be promising in slowing or possibly preventing neurodegenerative disorders.

Disruption of White Matter Integrity by Chronic Cerebral Hypoperfusion in Alzheimer’s Disease Mouse Model

2016 ◽  
Vol 52 (4) ◽  
pp. 1311-1319 ◽  
Author(s):  
Yun Zhai ◽  
Toru Yamashita ◽  
Yumiko Nakano ◽  
Zhuoran Sun ◽  
Ryuta Morihara ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Mouse Model ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
White Matter Integrity

Axon–glial disruption: the link between vascular disease and Alzheimer's disease?

2011 ◽  
Vol 39 (4) ◽  
pp. 881-885 ◽  
Author(s):  
Karen Horsburgh ◽  
Michell M. Reimer ◽  
Philip Holland ◽  
Guiquan Chen ◽  
Gillian Scullion ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
White Matter ◽  
Cognitive Decline ◽  
Vascular Dysfunction ◽  
Critical Role ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Early Event ◽  
Published Data

Vascular risk factors play a critical role in the development of cognitive decline and AD (Alzheimer's disease), during aging, and often result in chronic cerebral hypoperfusion. The neurobiological link between hypoperfusion and cognitive decline is not yet defined, but is proposed to involve damage to the brain's white matter. In a newly developed mouse model, hypoperfusion, in isolation, produces a slowly developing and diffuse damage to myelinated axons, which is widespread in the brain, and is associated with a selective impairment in working memory. Cerebral hypoperfusion, an early event in AD, has also been shown to be associated with white matter damage and notably an accumulation of amyloid. The present review highlights some of the published data linking white matter disruption to aging and AD as a result of vascular dysfunction. A model is proposed by which chronic cerebral hypoperfusion, as a result of vascular factors, results in both the generation and accumulation of amyloid and injury to white matter integrity, resulting in cognitive impairment. The generation of amyloid and accumulation in the vasculature may act to perpetuate further vascular dysfunction and accelerate white matter pathology, and as a consequence grey matter pathology and cognitive decline.

Chronic Cerebral Hypoperfusion Activates the Coagulation and Complement Cascades in Alzheimer's Disease Mice

Neuroscience ◽  
2019 ◽  
Vol 416 ◽  
pp. 126-136 ◽  
Author(s):  
Xiaowen Shi ◽  
Yasuyuki Ohta ◽  
Xia Liu ◽  
Jingwei Shang ◽  
Ryuta Morihara ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion

scholarly journals Clinical and Biophysical Principles of Vascular Dementia and Alzheimer’s Disease Treatment

2019 ◽  
Vol 5 (5) ◽  
pp. 57-72 ◽  
Author(s):  
S. Bulgakova ◽  
P. Romanchuk ◽  
A. Volobuev
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Hippocampal Neurons ◽  
Structural Changes ◽  
Neuronal Damage ◽  
Oxidant Stress ◽  
Cerebral Hypoperfusion ◽  
Term Care ◽  
Β Amyloid

Biophysics of blood circulation in Alzheimer’s disease is characterized by disorders of laminar blood flow and cerebral hypoperfusion. As a result, failure intracellular metabolism, there is a cascade of changes in neurons associated with the processes of excitotoxicity and oxidant stress, which in turn stimulates amyloidogenesis. Experimental and 25-year observations have shown that the long-existing state of hypoperfusion leads to hippocampal disorders. This process is accompanied by memory impairment, structural changes in the capillaries in the hippocampus, impaired glucose and protein metabolism, β–amyloid deposition, activation of glial tissue, death of hippocampal neurons. Neuroreflex disruption in the ‘cerebral heart’ and a violation of cerebrovascular homeostasis contributes to the development of vascular dementia through the following mechanisms, including cerebral microangiopathy, endothelial dysfunction, oxidative stress, neuronal damage, the increase in β–amyloid neurotoxicity, apoptosis, etc. The duration of therapy with antiglutamatergic and multimodal drugs in Alzheimer’s disease requires constant multidisciplinary monitoring of targets and medical and social control in the system of long-term care. Lifelong acquisition of knowledge, information positive Nano communication enable the preservation of mental health and active longevity. Innovative methods of P4-medicine of neuroplasticity management allow to carry out timely prevention of the factors reducing neuroplasticity, to keep factors of positive influence on visceral and cognitive brain, and the main thing — in due time to apply in practical health care the combined methods of preservation and development of the human cognitive brain.

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