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Research Articles and Papers on:

Alzheimer’s Disease

 

NEUROLOGY 2004;62:1967-1971
© 2004 American Academy of Neurology
Low thyroid-stimulating hormone as an independent risk factor for Alzheimer disease - Liesbeth A.D.M. van Osch, MSc, Eva Hogervorst, PhD, Marc Combrinck, FCP(SA) (Neurol) and A. David Smith, DPhil
Researchers wanted to see if there was a possible relationship between thyroid-stimulating hormone (TSH) levels, vascular risk factors, and Alzheimer disease (AD).

They measured TSH levels in 178  patients with Alzheimer’s Disease and 291 cognitively screened control subjects who were all euthyroid (TSH: 0.5 to 6 mU/L). Alzheimer’s  patients had significantly lower levels of TSH than control subjects. It was concluded that lowered TSH within the normal range is a risk factor for Alzheimer’s Disease. The article tells us that, “Low TSH levels could be a consequence of Alzheimer-related neuro-degeneration leading to reduced hypothalamic TRH secretion or decreased pituitary responsiveness and consequently low TSH levels. Low TSH or TRH levels could also precede dementia.” 


 

Thyroid Function and the Risk of Alzheimer Disease - The Framingham Study

Zaldy S. Tan, et al
Summarised from http://www.ncbi.nlm.nih.gov/pubmed/18663163 

Background: Clinical hypothyroidism and hyperthyroidism are recognized causes of reversible dementia, but previous studies relating thyrotropin (TSH) levels to cognitive performance in clinically euthyroid persons have yielded inconsistent results.  

Methods: We related TSH levels measured at baseline (March 1977-November 1979) to the risk of Alzheimer disease (AD) in 1864 cognitively intact, clinically euthyroid Framingham original cohort participants (mean age, 71 years; 59% women).  

Results: During an average follow-up of 12.7 years (range, 1-25 years), 209 participants (142 women) developed AD. Women in the lowest (<1.0 mIU/L) and highest (>2.1 mIU/L) tertiles (third) of TSH concentration were at increased risk for AD compared with those in the middle tertile. TSH levels were not related to AD risk in men. Analyses excluding individuals receiving thyroid supplementation did not significantly alter these relationships. In analyses limited to participants with TSH levels of 0.1 to 10.0 mIU/L, the U-shaped relationship between thyrotropin level and AD risk was maintained in women but not when analyses were limited to those with thyrotropin levels of 0.5 to 5.0 mIU/L.  

Conclusion: Low and high thyrotropin levels were associated with an increased risk of incident AD in women but not in men.