Abstract
The present study was aimed to investigate the relationships between thyroid stimulating hormone (TSH), freeT3 (fT3) and freeT4 (fT4) and brain glucose consumption as detectable by means of 2-deoxy-2-(F-18) fluoro-D-glucose (F-18 FDG) Positron Emission Tomography/Computed Tomography (PET/CT) in a selected population with Alzheimer disease (AD). We evaluated 87 subjects (37 males and 50 females, mean age 70 (±6) years old) with AD. All of them were subjected to TSH, fT3 and fT4 assay and to cerebrospinal fluid amyloid (Aβ1-42) and tau [phosphorylated-tau (p-tau) and total-tau (t-tau)] assay prior PET/CT examination. Values for TSH, fT3 and fT4 were in the normal range. The relationships were evaluated by means of statistical parametric mapping (SPM8) using age, sex, MMSE, scholarship and CSF values of amyloid and tau as covariates. We found a significant positive correlation between TSH values and cortical glucose consumption in a wide portion of the anterior cingulate cortex bilaterally (BA32) and left frontal lobe (BA25) (p FWE-corr <0.001; p FDRcorr <0.000; cluster extent 66950). No significant relationships were found between cortical F-18 FDG uptake and T3 and T4 serum levels. The results of our study suggest that a cortical dysfunction in anterior cingulate and frontal lobes may affect serum values of TSH in AD patients.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disorder leading to cognitive decline and dementia
The present study examined the correlation between thyroid stimulating hormone (TSH) levels within the normal range and cerebral glucose metabolism in patients with Alzheimer disease (AD), showing that serum TSH levels are positively correlated with glucose uptake in bilateral anterior cingulate cortex and left medial frontal gyrus
Literature evidence extensively explored the relationship between TSH levels and cognitive function, results are still conflicting
Summary
Alzheimer’s disease (AD) is a neurodegenerative disorder leading to cognitive decline and dementia. Paired-helical filaments of hyper-phosphorylated Tau compose the neuro-fibrillary tangles[2, 3] These pathological structures are usually located inside dendrites and linked from the neuropil through dendritic shafts to the neuronal cell bodies which contain the neuro-fibrillary tangles[4]. It is suggested that the pathological aggregation of these proteins is related to neuronal toxicity and cell loss, since Tau aggregate spreading in AD brain increases with cognitive decline[5]. In patients with MCI, low TSH correlated with the risk of developing AD in a 6-years follow-up study[18]. Aim of this study was to investigate the relationships among TSH, fT3 and fT4 and brain glucose consumption as detectable by means of F-18 FDG PET/CT in a population with clinical diagnosed AD
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