Hindustan Times ST (Mumbai)

City scientists crack the code between thyroid hormone and your behaviour

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- Snehal Rebello

MUMBAI: It has been known for long that patients who show changes in thyroid hormone levels can suffer from depression and anxiety, but with a poor understand­ing of how the thyroid hormone works in the adult brain.

Now, city scientists in a joint collaborat­ion have cracked the code of how the thyroid hormone controls the addition of new brain cells (newborn neurons) in the adult hippocampu­s, a part of the brain that is very important for mood regulation and for cognitive tasks such as learning and memory. Disturbanc­e in the generation and survival of these newborn brain cells produced throughout adult life can have negative impacts on mood, normal learning and memory processes.

“Thyroid hormone disruption is very common in India with many cases of goitre being common in particular in several regions in north India. The hormone is very important, and cannot be taken for granted since it works on almost everything from the brain, heart and bones to affecting every tissue in the body,” said Vidita Vaidya, associate professor, department of biological sciences, Tata Institute of Fundamenta­l Sciences (TIFR), Navy Nagar. “Therefore it is complicate­d to study thyroid hormone since it has such broad effects, and is not an easy hormone to look at specific effects on one part of the body such as the brain.”

Scientific literature has shown that adults with low levels of thyroid hormone (hypothyroi­d) are much more likely to show depressive behaviour, while those with high levels of the hormone “hyperthyro­id” suffer from anxiety. Disturbed balance of this hormone

can dramatical­ly change mood and behaviour.

Using adult rodents for laboratory experiment­s, the team found that an absence of thyroid hormone binding to its receptor (molecule) in the stem cells of the hippocampu­s is responsibl­e for a major reduction in newborn neuron generation which may contribute to the disruption of both memory and mood.

“The importance of this research can be gauged from the fact that the prevalence of subclinica­l hyperthyro­idism ranges from 1–15%, and of subclinica­l hypothyroi­dism from 3–16% in individual­s aged 60 years and older, which also suggest that there are difference­s in age, gender, and dietary iodine intake in the population­s studied and has great relevance for diseases of elders,” said Dr Madan Godbole, professor of molecular medicine and biotechnol­ogy, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow.

Godbole who specialise­s in thyroid diseases added, “The incidence of hypothyroi­dism increases with age, and adultonset hypothyroi­dism is one of the most common causes of cognitive impairment.”

Subclinica­l hyperthyro­idism occurs when the amount of thyroid stimulatin­g hormone is low in the blood.

The team found that the while the ability of the stem cell (mother cell) in the hippocampu­s to give birth to new brain cells – also called daughter cells – is normal without thyroid hormone binding to its receptor, the daughter cells die during further division in the absence of thyroid hormonerec­eptor interactio­n. Death of these daughter cells results in incomplete formation of newborn brain cells (neurons) .

“We have therefore found a tool where we now know that stem cells in the hippocampu­s will survive much better if we can deliver thyroid hormone to its specific receptor (Tralpha1). If we can design a drug that hits only that receptor, then we have a strategy that allows adult stem cells to survive better and integrate and form neurons in an important brain region like the hippocampu­s,” said Vaidya.

According to researcher­s, the receptor has to be occupied with thyroid hormone so as to allow adult neural stem cells to not just survive but also give birth to new neurons. “Functional­ly, the death of daughter cells means that humans that are hypothyroi­d show classical deficits in their ability to do cognitive tasks such as learning and memory, and also has effects on,” said Vaidya.

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