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How vitamin D deficiency may compromise immune function: Tau protein, glutamate

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Older individuals who are vitamin D deficient also tend to have compromised immune function, according to new research accepted for publication in the Endocrine Society's Journal of Clinical Endocrinology & Metabolism. The study, "Vitamin D Deficiency is Associated with Inflammation in Older Irish Adults," is now published online, ahead of print in the The Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM).

Vitamin D deficiency may compromise immune function. Vitamin-deficient seniors are more likely to have biomarkers for heart disease and inflammation says a new study. Older individuals who are vitamin D deficient also tend to have compromised immune function, according to the new research.

Vitamin D plays an important role in helping the body absorb calcium needed for healthy bones

The skin naturally produces vitamin D when it is exposed to sunlight. People also obtain smaller amounts of the vitamin through foods, such as milk fortified with vitamin D. More than 1 billion people worldwide are estimated to have deficient levels of vitamin D due to limited sunshine exposure.

"Our data suggest vitamin D may be involved in maintaining the health of the immune system as well as the skeletal system," said one of the study's authors, Mary Ward, PhD, of the University of Ulster in Coleraine, U.K, according to the February 25, 2014 news release, Vitamin D deficiency may compromise immune function. "This study is the first to find a connection between vitamin D levels and inflammation in a large sample of older individuals." The observational study of 957 Irish adults who were at least 60 years old examined vitamin D levels as well as biomarkers of inflammation.

Participants who were vitamin D deficient were more likely to have high levels of these biomarkers, which are linked to cardiovascular disease and inflammatory conditions such as multiple sclerosis and rheumatoid arthritis

"The results indicate immune function may be compromised in older individuals with vitamin D deficiency," Ward said in the news release. "Ensuring older individuals have optimal vitamin D levels may be a way to boost immune function in this population, but this needs to be confirmed through additional studies."

Other authors of the study include: E. Laird and A.M. Molloy of Trinity College in Dublin, Ireland; H. McNulty, L. Hoey, E. McSorley, J.M.W. Wallace, E. Carson and J.J. Strain of the University of Ulster; and M. Healy, M. Casey and C. Cunningham of St. James's Hospital in Dublin.

Founded in 1916, the Endocrine Society is the world's oldest, largest and most active organization devoted to research on hormones and the clinical practice of endocrinology. Today, the Endocrine Society's membership consists of over 17,000 scientists, physicians, educators, nurses and students in more than 100 countries. Society members represent all basic, applied and clinical interests in endocrinology. The The Endocrine Society is based in Washington, DC. You also can follow the Endocrine Society on Twitter.

How increased brain cell activity boosts brain fluid levels of a protein linked to Alzheimer's disease

Increased brain cell activity boosts brain fluid levels of a protein linked to Alzheimer’s disease, according to new research in another study from scientists at Washington University School of Medicine in St. Louis. The study, "Neuronal activity regulates extracellular tau in vivo," is published online since February 18, 2014 in the Journal of Experimental Medicine. Tau protein is the main component of neurofibrillary tangles, one of the hallmarks of Alzheimer’s disease. It has been linked to other neurodegenerative disorders, including frontotemporal dementia, supranuclear palsy and corticobasal degeneration.

“Healthy brain cells normally release tau into the cerebrospinal fluid and the interstitial fluid that surrounds them, but this is the first time we’ve linked that release in living animals to brain cell activity,” said senior author David M. Holtzman, MD, according to the February 25, 2014 news release, Brain cell activity regulates Alzheimer’s protein . “Understanding this link should help advance our efforts to treat Alzheimer’s and other neurodegenerative disorders associated with the tau protein.

Tau protein stabilizes microtubules, which are long columns that transport supplies from the center of the cell to the distant ends of the cell’s branches

Some tau in the cell is not bound to microtubules. This tau can become altered and clump together inside brain cells, forming structures called tangles. Scientists have tracked the spread of these clumps through brain networks in animal models.

“In Alzheimer’s disease, you first see clumps of tau in a region called the entorhinal cortex, and then in the hippocampus, and it continues to spread through the brain in a regular pattern,” said Holtzman, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology, according to the news release. “In another disorder, supranuclear palsy, tau clumps first appear in the brain stem and then spread to regions that the brain stem projects to.”

These regular patterns of tau spread through brain networks have led scientists to speculate that dysfunctional tau travels to different brain regions via synapses — the areas where individual nerve cells communicate with each other.

Holtzman’s results support this hypothesis, showing that when nerve cells “talk” to each other, tau levels go up in the fluids between those cells, suggesting that brain cells are secreting tau when they send signals. So far, the researchers only have been able to measure single copies of tau in brain fluid, not the tau clumps. They are looking for a way to detect the clumps.

If brain cells can secrete and take in clumps of tau, the scientists believe, these clumps may cause previously normal tau in the receiving cell to become corrupted, fostering the spread of a form of tau involved in disease. “We also want to know whether brain cells are secreting tau as waste or if tau has a function to perform outside the cell,” Holtzman said in the news release. “For example, there have been hints that tau may modulate how easy or difficult it is to get brain cells to communicate with each other.”

The Tau Consortium and the Japan Society for the Promotion of Science supported the study. Authors are Yamada K, Holth JK, Liao F, Stewart FR, Mahan TE, Jiang H, Cirrito JR, Patel TK, Hochgräfe K, Mandelkow E-M, and David M. Holtzman. You can check out the abstract of the study online, "DM. Neuronal activity regulates extracellular tau in vivo," published online February. 18, 2014 in the Journal of Experimental Medicine.

Tau is primarily a cytoplasmic protein that stabilizes microtubules, according to the study's abstract

What happens is that tau also is found in the extracellular space of the brain at appreciable concentrations. Researchers are trying to understand more about tau. Although its presence there may be relevant to the intercellular spread of tau pathology, the cellular mechanisms regulating tau release into the extracellular space are not well understood. That's why the research focused on testing the context of neuronal networks.

To test this in the context of neuronal networks in vivo, the researchers used in vivo microdialysis. Increasing neuronal activity rapidly increased the steady-state levels of extracellular tau in vivo.

How does glutamate play a role?

Importantly, the researchers write in the study's abstract, presynaptic glutamate release is sufficient to drive tau release. Although tau release occurred within hours in response to neuronal activity, the elimination rate of tau from the extracellular compartment and the brain is slow (half-life of ~11 d). The in vivo results provide one mechanism underlying neuronal tau release and may link trans-synaptic spread of tau pathology with synaptic activity itself.

For the general consumer, such as a senior citizen looking for more information on the role glutamate plays in brain activity, you also may be interested in taking a look at the site, "The role of glutamate in dementia."

Glutamate is an excitatory neurotransmitter, but may also act as an endogenous neurotoxin, notes that study's abstract. There is good evidence for an involvement of the glutamatergic system in the pathophysiology of dementia.

The glutamatergic transmission machinery is quite complex and provides a gallery of possible drug targets. There are good arguments both for an agonist and an antagonist strategy. When following the antagonist strategy, the goal is to provide neuroprotective effects via glutamate receptor antagonisms without inhibiting the physiological transmission that is required for learning and memory formation.

The study's abstract explains that when following the agonist strategy, the goal is to activate glutamatergic transmission without neurotoxic side effects. Several available antidementia drugs may modulate the glutamatergic transmission. Fascinating topic how glutamate works in the brain. You may wish to check out the site, "Everything You Need To Know About Glutamate And Monosodium Glutamate."

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