Vascular Dementia and Cognitive Impairment

Stroke ◽  
2022 ◽  
pp. 221-236.e8
Author(s):  
Sudha Seshadri ◽  
Michelle R. Caunca ◽  
Tatjana Rundek
Author(s):  
Amteshwar Singh Jaggi

Aim: The aim of the present study is to explore the neuroprotective effects of remote ischemic preconditioning in long term cognitive impairment after global cerebral ischemia induced-vascular dementia in mice. Material and methods: The mice were subjected to global cerebral ischemia by occluding the bilateral common carotid arteries for 12 minutes followed by the 24 hours of the reperfusion. The remote ischemic preconditioning stimulus was delivered in the form of 4 cycles of ischemia/reperfusion for 5 minutes each. The cerebral ischemic injury induced-long term cognitive impairment-related learning and memory alterations was assessed using morris water maze, the motor performances of the animals were evaluated using rota-rod test and neurological severity score. The cerebral infract size of the brain were quantified using triphenyltetrazolium chloride staining. Results: Global cerebral ischemia causes long term memory impairment, decreases motor performances and increases the brain infract size in animals. The delivery of remote ischemic preconditioning stimulus significantly abolished the long-term cognitive impairment and ameliorates the motor performances as well as cerebral infract size in brain. Conclusion: The remote ischemic preconditioning mediates neuro protection against global cerebral ischemic injury induced long-term cognitive impairment.


Author(s):  
Victoria J. Williams ◽  
Steven E. Arnold ◽  
David H. Salat

Throughout the lifespan, common variations in systemic health and illness contribute to alterations in vasculature structure and function throughout the body, significantly increasing risk for cardiovascular and cerebrovascular disease (CVD). CVD is a prevalent cause of mortality in late life; it also promotes brain alterations, contributing to cognitive decline and, when severe, vascular dementia. Even prior to diseased states, individual variation in CVD risk is associated with structural and functional brain alterations. Yet, how cumulative asymptomatic alterations in vessel structure and function contribute to more subtle changes in brain tissue integrity and function that emerge in late life is unclear. Finally, vascular risk factors are associated with the clinical progression of neurodegenerative diseases such as Alzheimer’s disease (AD); however, recent theory posits that vascular degeneration may serve a contributory role in these conditions. This chapter reviews how lifespan changes in vascular health contribute to degenerative changes in neural tissue and the subsequent development of cognitive impairment and/or vascular dementia. It first discusses associations between vascular risk factors and cognition and also how declining vascular health may lead to cognitive impairment and dementia. Next, it identifies basic aspects of cerebrovascular anatomy and physiology sustaining tissue health and discusses how vulnerabilities of this system contribute to neurodegenerative changes. Finally, it reviews evidence of vascular contributions to AD and presents ideas for future research to better understand the full spectrum of cerebrovascular contributions to brain aging, cognitive decline, and dementia.


2020 ◽  
Vol 45 (2) ◽  
Author(s):  
Arpita Chakraborty ◽  
Samir Kumar Praharaj ◽  
R. V. Krishnananda Prabhu ◽  
M. Mukhyaprana Prabhu

AbstractBackgroundMore than half portion of the brain is formed by lipids. They play critical roles in maintaining the brain's structural and functional components. Any dysregulation in these brain lipids can lead to cognitive dysfunction which are associated with neurological disorders such as Alzheimer's disease, Parkinson's disease, schizophrenia, vascular dementia etc. Studies have linked lipids with cognitive impairment. But not much has been studied about the complex brain lipids which might play a pivotal role in cognitive impairment. This review aims to highlight the lipidomic profiles in patients with cognitive dysfunction.ResultsForty-five articles were reviewed. These studies show alterations in complex lipids such as sphingolipids, phospholipids, glycolipids and sterols in brain in various neurological disorders such as vascular dementia, Parkinson's and Alzheimer's disease. However, the classes of fatty acids in these lipids involved are different across studies.ConclusionsThere is a need for targeted lipidomics analysis, specifically including sphingolipids in patients with neurodegenerative disorders so as to improve diagnostics as well as management of these disorders.


Neurocase ◽  
2012 ◽  
Vol 20 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Doo Sang Yoon ◽  
Kihyo Jung ◽  
Geon Ha Kim ◽  
Sook Hui Kim ◽  
Byung Hwa Lee ◽  
...  

2021 ◽  
Vol 36 (6) ◽  
pp. 1023-1023
Author(s):  
Amanda M Wisinger ◽  
Matthew S Phillips ◽  
Dustin A Carter ◽  
Kyle J Jennette ◽  
Joseph W Fink

Abstract Objective Studies that have used semantic fluency tasks to guide differential diagnosis of Alzheimer’s disease (ad) and vascular dementia (VaD) typically only examine the total number of words produced, which has yielded conflicting results. The present study examined whether other indices of semantic fluency (i.e., clustering and switching), which are thought to better isolate the components of semantic memory and executive functioning abilities, would discriminate among ad, VaD, and mild cognitive impairment (MCI). Method A retrospective sample of 156 patients (mean age = 78.64; 76.3% female, 23.7% male; 26.9% White, 71.2% Black, 1.9% Other) who completed a comprehensive neuropsychological evaluation as part of a workup related to memory concerns and were diagnosed with ad, VaD, or MCI was utilized. Separate univariate analyses of variance were used to examine group differences on three indices of semantic fluency (animals): total words, mean cluster size, and number of switches. Results There was a significant main effect of group for total words [F(2,153) = 7.09, p = 0.001], mean cluster size [F(2, 153) = 3.44, p = 0.035] and number of switches [F(2,153) = 3.36, p = 0.037]. Bonferroni post-hoc tests revealed that the ad and VaD groups produced significantly fewer total words than the MCI group, the ad group produced significantly smaller clusters than the VaD group, and the VaD group produced significantly fewer switches than the MCI group. Conclusion Observed group differences suggest that clustering and switching may aid in discriminating between dementia etiologies. Future studies may benefit from examining the association between these fluency indices and performance on executive functioning and semantic knowledge tasks to better understand these findings.


Author(s):  
Charles Alessi ◽  
Larry W. Chambers ◽  
Muir Gray

Ageing is not a cause of major problems till the later nineties. The problems we fear—dementia, disability, and dependency are due to three other processes: loss of physical fitness, which starts long before old age, diseases, many of which are preventable, and pessimistic attitudes. Both lay people and our professional colleagues have difficulty with the meanings of dementia, Alzheimer’s disease, vascular dementia, and cognitive ageing and use these terms in different ways, often incorrectly. Now is the time to use your assets—preserving and increasing your brain reserve to reduce your risk of dementia. The fitness gap can be closed at any age by increasing both physical and social activity. There is no upper age limit for prevention. The steps we recommend for reducing the risk of dementia will also help you reduce the risk of other diseases, keep you fitter, and help you feel better, and are equally relevant for people who have already developed mild cognitive impairment or dementia.


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