According to the United Nations the aging population is growing and by 2050 the number of people aged 60 years old will reach 2 billion worldwide. With the aging population the prevalence of age-related disease is predicted to increase. An example of an age-related disease is neurodegeneration.  Dementia can be a result of several pathologies including increased levels of Lewy bodies (abnormal aggregates of protein in nerve cells), as seen in Parkinson’s disease.

Cerebrovascular disease is the second most common cause of dementia and is a result of  changes in blood flow to or within the brain. Blood flow in the brain can change because of hypertension, diabetes, smoking, and hypercholesterolemia. Patients with cerebrovascular disease experience cognitive impairment, specifically when trying to remember things or plan events/trips. It is important to note that symptoms can vary from patient to patient. A type of cerebrovascular disease is vascular cognitive impairment (VCI).

Nutrition is a modifiable risk factor for diseases of aging. As people age their ability to absorb nutrients from their diet decreases.  Several studies have reported that changes in B-vitamin absorption may play a role in the onset and progression of dementia. Additionally, a study by researchers in the United Kingdom shows that B-vitamin supplementation reduced brain volume loss in areas associated with cognitive decline. A recent international consensus statement from leaders in the field suggests that deficiencies in B-vitamin metabolism should be considered when screening dementia patients. My research using model organisms has tried to understand the disease processes associated with dementia.

Using a mouse model of VCI we have reported that deficiencies in folic acid, either dietary or genetic affect the onset and progression of VCI. Using the Morris water maze task we report that mice with VCI and folate deficiency performed significantly worse compared to controls. We assessed changes in the brain using MRI and interestingly found that folate deficiency changed the vasculature in the brains of mice with VCI. Because of either a genetic or dietary folate deficiency all the mice had increased levels of homocysteine.

Our results suggest that it is not elevated levels of homocysteine making the brain more vulnerable to damage, but the deficiency in folic acid, either dietary or genetic, that changes the brain. In the cell folic acid is involved in DNA synthesis and repair as well as methylation. These are vital functions for normal cell function. Therefore, reduced levels of folate may be changing the cells in the brain and making them more vulnerable to certain types of damage. We think that high levels of homocysteine may just be an indication of some deficiency (e.g. reduced dietary intake of folic acid). Maintaining normal levels of homocysteine are needed, since studies in humans have shown that elevated levels of homocysteine are a risk factor for neurodegenerative diseases and that reducing them is beneficial.

 

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