Dutch researchers have uncovered evidence that argues against an important role for thyroid function in the development of Alzheimer's disease (AD).
Writing in the Journal of Clinical Endocrinology & Metabolism, the study authors explain that previous reports have linked thyroid function to the development of AD.
These have shown AD patients to have more atrophy of the hippocampus and amygdala in comparison with healthy elderly individuals; both of which contain "a high density of thyroid hormone receptors and are an important target of thyroid hormones entering the brain," they emphasize.
However, Monique Breteler, from Erasmus Medical Center in Rotterdam, and colleagues note: "Although thyroid dysfunction could be related to clinical symptoms of AD, the underlying mechanism is unclear."
To address this issue, the investigators followed up 1025 individuals aged 60-90 years from a population-based cohort that began in 1995-1996 and lasted until 2005.
They assessed each participants' levels of thyroid stimulating hormone (TSH) and thyroid hormones free thyroxine (fT4), 3,5,3'-triiodothyronine (T3) and 3,3,5'-triiodothyronine (rT3).
During the study period, 63 individuals were diagnosed with dementia, and 46 of these were cases of AD.
However, results indicated that there was no relationship between levels of TSH and thyroid hormones and the risk of AD.
Magnetic Resonance Imaging analyses in a subset of 489 patients showed that TSH and thyroid hormone levels were not related to brain atrophy. Moreover, non-demented individuals with high fT4 and rT3 levels had more hippocampal and amygdalar atrophy than those with dementia.
"In this community sample, there was no relation between thyroid function and the risk of dementia or AD," Breteler et al conclude.
"Future studies are needed to elucidate whether the association of higher fT4 and rT3 levels with brain atrophy on MRI has functional significance," they suggest.