Contribution of cerebral microvascular mechanisms to age-related cognitive impairment and dementia

Fang, Xing; Crumpler, Reece F.; Thomas, Kirby N; Mazique, Jena' N; Roman, Richard J.; Fan, Fan

doi:10.1556/2060.2022.00020

Cited by 14 publications

(12 citation statements)

References 55 publications

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“…Oxidative stress is also associated with long-term cognitive impairment [85,86]. Herein, oxidative stress marker levels were enhanced after SAE and EE could reduce these increases.…”

Section: Discussionmentioning

confidence: 84%

Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy

Tang¹,

Duan²,

Ge³

et al. 2022

J. Integr. Neurosci.

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Background: One of the most serious complications of sepsis is sepsis-associated encephalopathy (SAE), which impairs the cognition ability of survivors. Environmental enrichment (EE) has been demonstrated to alleviate cognition deficits under many kinds of brain injury conditions. However, EE's effects on SAE remain unknown. Therefore, this study aimed to determine EE's effect on cognition disorders under SAE conditions and the underlying mechanism. Materials and Methods: Adult male rats, subject to SAE or not, were housed under a standard environment (SE) or EE for 30 days. Subsequently, the rats were subjected to cognitive tests, such as the novel object recognition (NOR) test, the Morris water maze (MWM) test, an Open Field (OF) test, the elevated plus maze (EPM) test, and a sensory neglect (SN) test. Neuroinflammation, apoptosis, and oxidative stress changes in the brain were also detected. Results: The results revealed that SAE impaired somatesthesia, recognition memory, spatial learning and memory, and exploratory activity, which were significantly improved by EE housing. EE also prevented SAE-induced anxiety-like behavior. In addition, EE housing capable induced a decrease in pro-inflammatory cytokines, and an increase in anti-inflammatory cytokines and antioxidant properties in the brain. Moreover, EE housing exerted an anti-apoptosis function by upregulating the level of B-cell lymphoma/leukemia-2 (Bcl-2) level and downregulating the level of p53 level in the hippocampus. Conclusions: The results of the present study indicated that EE exerts a neuroprotective function on cognitive ability in SAE rats. The effect is achieved by increasing antioxidants, and anti-inflammatory and antiapoptotic capacities. EE can effectively rescue SAE-induced cognitive deficits.

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“…Oxidative stress is also associated with long-term cognitive impairment [85,86]. Herein, oxidative stress marker levels were enhanced after SAE and EE could reduce these increases.…”

Section: Discussionmentioning

confidence: 84%

Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy

Tang¹,

Duan²,

Ge³

et al. 2022

J. Integr. Neurosci.

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“…AD/ADRD is the most costly disease and one of the major causes of disability and morbidity in the elderly worldwide 1 . Although Aβ and Tau abnormality, neuro-inflammation, and oxidative stress have been considered to be the driving forces of AD/ADRD, more than 50% of AD/ADRD patients have mixed brain pathologies 3,16 . Cholinesterase inhibitors, approved by the U.S. Food and Drug Administration (FDA) for AD treatments for AD, only alleviate AD symptoms by temporarily improving memory and cognition.…”

Section: Discussionmentioning

confidence: 99%

“…AD/ADRD is the most costly disease and one of the major causes of disability and morbidity in the elderly worldwide 1 . Although Aβ and Tau abnormality, neuroinflammation, and oxidative stress have been considered to be the driving forces of AD/ADRD, more than 50% of AD/ADRD patients have mixed brain pathologies 3,16 .…”

Section: Discussionmentioning

confidence: 99%

“…Emerging studies demonstrated that brain hypoperfusion is an early and persistent symptom of AD and AD-related dementias (ADRD) [2][3][4][5][6] . Reduced perfusion in the neocortex and hippocampus has been reported to promote neuronal damage and dementia associated with poor cerebral blood flow (CBF) autoregulation, blood-brain barrier (BBB) leakage, and dysfunction of the neurovascular unit (NVU) in AD and aging, hypertension, and diabetes-related dementia [7][8][9][10][11][12][13][14] .…”

Section: Introductionmentioning

confidence: 99%

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Longitudinal Characterization of Cerebral Hemodynamics in the TgF344-AD Rat Model of Alzheimer’s Disease

Fang

Tang

Zhang

et al. 2022

Preprint

Self Cite

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Alzheimer's Disease (AD) is a global healthcare crisis. The TgF344-AD rat is an AD model exhibiting age-dependent AD pathological hallmarks. We confirmed that AD rats developed cognitive deficits at 6 months without alteration of any other major biophysical parameters. We longitudinally characterized cerebral hemodynamics in AD rats at 3, 4, 6, and 14 months. The myogenic responses of the cerebral arteries and arterioles were impaired at 4 months of age in the AD rats. Consistent with the ex vivo results, the AD rat exhibited poor autoregulation of surface and deep cortical cerebral blood flow two months preceding cognitive decline. The dysfunction of cerebral hemodynamics in AD is exacerbated with age associated with reduced cerebral perfusion. Further, abolished cell contractility contributes to cerebral hemodynamics imbalance in AD. This may be attributed to enhanced ROS production, reduced mitochondrial respiration and ATP production, and disrupted actin cytoskeleton in cerebral vascular contractile cells.

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“…So, cerebral microvascular inflammation likely accelerated cognitive impairment in the elderly with AD under HTN. 120 …”

Section: Pathogenesis Of Hypertension and Alzheimer’s Disease: Experi...mentioning

confidence: 99%

Pathophysiological Association of Alzheimer’s Disease and Hypertension: A Clinical Concern for Elderly Population

Yao¹,

Jiang²,

Lin³

et al. 2023

CIA

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Alzheimer’s disease (AD), the most common cause of dementia and the fifth leading cause of death in the adult population has a complex pathophysiological link with hypertension (HTN). A growing volume of published literature on a parallel elevation of blood pressure (BP), amyloid plaques, and neurofibrillary tangles formation in post-middle of human brain cells has developed new, widely accepting foundations on this association. In particular, HTN in elderly life mediates cerebral blood flow dysfunction, neuronal dysfunction, and significant decline in cognitive impairment, primarily in the late-life populace, governing the onset of AD. Thus, HTN is an established risk factor for AD. Considering the impact of AD, 1.89 million deaths annually, and the failure of palliative therapies to cure AD, the scientific research community is looking to adopt integrated approaches to target early modified risk factors like HTN to reduce AD burden. The current review highlights the significance and impact of HTN-based prevention in lowering the AD burden in the elderly by providing a comprehensive overview of the physiological relationship between AD and HTN with an in-detail explanation of the role and applications of pathological biomarkers in this clinical association. The review will gain worth in presenting new insights and providing inclusive discussion on the correlation between HTN and cognitive impairment. It will increase across a wider scientific audience to expand understanding of this pathophysiological association.

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Contribution of cerebral microvascular mechanisms to age-related cognitive impairment and dementia

Cited by 14 publications

References 55 publications

Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy

Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy

Longitudinal Characterization of Cerebral Hemodynamics in the TgF344-AD Rat Model of Alzheimer’s Disease

Pathophysiological Association of Alzheimer’s Disease and Hypertension: A Clinical Concern for Elderly Population

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