Dementia is a general term for a group of conditions where brain function worsens over time. As the condition progresses, the ability to remember, think, interact socially, make decisions and lead an independent life decreases. Worldwide, there are 50 million people with dementia and “10 million new cases every year”. Dementia is a major cause of disability in older people and is the main reason they become dependent on others. The social and economic burden of the condition also affects carers, families and the wider community. Most cases of dementia are not caused by Alzheimer’s disease, which recognizes a certain genetic cause. Conditions that directly or indirectly damage the brain – such as stroke – are the most common causes of dementia. All conditions that affect the small blood vessels of the brain contribute to dementia and stroke. The disease in question is called chronic cerebrovasculopathy (CSVD).
A few years ago, researchers identified a mechanism by which the blood vessel changes from CSVD to damage the myelin of nerve fibers that carry signals between brain cells. The scientists also showed how certain drugs reversed blood vessel changes and prevented nerve fiber damage in the rats’ brains. CT brain scans of individuals with dementia often show abnormalities in the white matter, which consists mainly of nerve fibers and their myelin covering. But until this study, the underlying mechanisms involving CSVD as a driver of myelin damage in white matter were unknown. If the mechanism were the same in human CSVD, these findings could pave the way for new treatments for dementia and stroke. In fact, suppressing damaging changes in blood vessels helps keep nerve cells functioning longer.
CSVD is common among older individuals, not only does it directly cause stroke and dementia, but can also worsen the effects of Alzheimer’s disease and lead to depression and gait problems. For a long time, it was thought that the different features of CSVD were signs of different types of tissue changes. But more recently, scientists have realized that these features likely share many similar changes affecting small blood vessels. And, as neuroimaging technology advances, they are finding it easier to explore the underlying mechanisms. The team found that CSVD causes dysfunction of endothelial cells, which are the cells that form the inner lining of blood vessels. When the endotheliums become dysfunctional, preventing precursor cells from maturing into cells that form the myelin covering on nerve fibers. It is the arterial capillaries, in fact, that carry the nourishment to the myelin to be built.
Further investigation revealed that rats that developed CSVD in laboratory-induced models had a mutated form of an enzyme called ATPase, which led to dysfunction of their endothelial cells. The mutation was also found in human brain tissue samples with CSVD from deceased patients. In a final set of experiments, the scientists showed how the use of drugs to stabilize endothelial cells could reverse white matter abnormalities in CSVD early in the rat model, suggesting a potential therapeutic approach. There are known possibilities of protecting blood vessels with external interventions. Currently in cerebrovasculopathies with stabilized dementia, clinical prescriptions serve only as a complement and include supplements based on Gingko biloba, blueberry extract, choline or aminoacid derivatives and polysaccharides called glycans (GAGs). But not many results are achieved once cognitive functions are permanently impaired.
But the alterations of the blood vessels come with hypertension, diabetes, cigarette smoking and other voluntary or not wrong daily habits. Not surprisingly, the highest percentage of patients with cognitive impairment is among chronic heart patients and diabetics with little responsible diabetes management. There are currently no drugs that slow or stop Alzheimer’s-type dementia and no treatments to help people living with vascular dementia. Hence, it is very much up to us to pave the way or prevent cerebrovasculopathy in the future.
- Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
Kandiah N et al. CNS Neurosci Ther. 2019; 25(2):288-298.
Zhang QY et al. Oxid Med Cell Longev. 2019; 2019:7850154.
Abdullahi W et al. Am J Physiol Cell Physiol. 2018 Jun 27.
Horsburgh K et al. Clin Sci (Lond). 2018; 132(8):851-868.
Dott. Gianfrancesco Cormaci
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