The pathobiology of neurovascular aging

 

What will your competent? doctor do with this to ensure you DON'T GET DEMENTIA from your extra risk from your stroke? NOTHING? So, you DON'T have a functioning stroke doctor, do you? Why the hell doesn't the board of directors' have policies to remove incompetent doctors? They also must be fucking incompetent!

Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely refute all my points with NO EXCUSES!! And what is your definition of competence in stroke? Swearing at me is allowed, I'll return the favor. Don't even attempt to use the tyranny of low expectations as an answer.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

The pathobiology of neurovascular aging

Monica M. Santisteban¹ monica.santisteban@vumc.org ∙ Costantino Iadecola² coi2001@med.cornell.edu

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Summary

As global life expectancy increases, age-related brain diseases such as stroke and dementia have become leading causes of death and disability. The aging of the neurovasculature is a critical determinant of brain aging and disease risk. Neurovascular cells are particularly vulnerable to aging, which induces significant structural and functional changes in arterial, venous, and lymphatic vessels. Consequently, neurovascular aging impairs oxygen and glucose delivery to active brain regions, disrupts endothelial transport mechanisms essential for blood-brain exchange, compromises proteostasis by reducing the clearance of potentially toxic proteins, weakens immune surveillance and privilege, and deprives the brain of key growth factors required for repair and renewal. In this review, we examine the effects of neurovascular aging on brain function and its role in stroke, vascular cognitive impairment, and Alzheimer’s disease. Finally, we discuss key unanswered questions that must be addressed to develop neurovascular strategies aimed at promoting healthy brain aging.

Keywords

1. neurovasculome
2. neurovascular unit
3. blood-brain barrier
4. vascular cognitive impairment
5. Alzheimer’s disease
6. rejuvenation strategies

Introduction

The world population is aging at an unprecedented rate, making it a public health priority to improve the quality of life by preventing or minimizing the impact of age-related diseases.¹ Comprehensive global estimates of disease burden and mortality have shown that the increase in life expectancy has led to a shift from communicable to non-communicable diseases as the major causes of death and disability.^2,3 Given the chronic course of non-communicable diseases, the world population lives longer but in poorer overall health.³ Neurovascular diseases, such as stroke and dementia, are major culprits of the deteriorating quality of life of the elderly. Every year, 15 million people have a new stroke worldwide, 30% of whom survive with long-term physical or cognitive disabilities that negatively impact activities of daily living (https://www.emro.who.int/health-topics/stroke-cerebrovascular-accident/index.html). In addition, 55 million people worldwide are living with dementia, mainly vascular cognitive impairment dementia (VCID) and Alzheimer’s disease (AD) (https://www.alzint.org/about/dementia-facts-figures/dementia-statistics/), conditions that often overlap and in which vascular factors play a pathogenic role.^4,5 Therefore, it has become increasingly apparent that brain health critically depends on neurovascular health,⁶ and gaining a better understanding of how aging alters the neurovasculature may help develop new strategies to promote healthy brain aging and improve the quality of life in old age⁷ (“adding life to years”).

Aging induces profound alterations in all segments of the neurovasculature, from the large blood vessels in the neck to the intracranial, meningeal, and lymphatic vasculature. These alterations have long been known to play a critical role in brain diseases of old age and have been a topic of intense study for decades.⁸ Seminal advances in the biology of aging have provided a deeper understanding of the integrated drivers of organismal aging, such as genomic alterations, chronic inflammation, cellular senescence, extracellular matrix (ECM) remodeling, stem cell exhaustion, and others.⁹ These processes have a profound impact on the neurovasculature, and cerebrovascular aging has emerged as a key determinant of brain aging and associated diseases.¹⁰ At the same time, advances in brain imaging and the recent introduction of single-cell or single-nuclei transcriptomics have provided new insights into the intimate relationships between the brain and its vasculature in health and disease. These advances have shed new light on the influence of aging on neurovascular and neurodegenerative diseases.

Here, we seek to provide a critical appraisal of these new developments and their significance for brain health and for the risk for neurological diseases of old age. After briefly reviewing basic concepts on the structure and function of the neurovasculature and the biology of aging, the vascular changes induced by “healthy aging” will be examined. These findings will be integrated with data emerging from single-cell or single-nuclei molecular studies of aging vessels aimed at identifying the cell types and related signaling mechanisms driving age-related changes. Finally, the impact of the vascular changes on disease risk will be examined, focusing on highly prevalent conditions associated with cognitive decline and on rejuvenation strategies to support healthy brain aging by promoting neurovascular health.

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