Thyroid function, the risk of dementia and neuropathologic changes: The Honolulu-Asia Aging Study

(2) In the current study, the lack of data on treatment and the effects of treatment on thyroid dysfunction limited a more rigorous analysis. (3) Some other factors may influence the concentration of TSH, such as pituitary-related disease (40). (4) The heterogeneity of results may be due to differences in race, method of TSH measurement, and the definition of thyroid dysfunction. Owing to inadequate information, it was difficult to analyze the heterogeneity further.

Data were obtained from participants enrolled in longitudinal studies at the Washington University in St. Louis School of Medicine’s Alzheimer’s Disease Research Center (ADRC). These longitudinal studies were initiated in 1979, and include participants with no cognitive impairment as well as dementia. Participants are volunteers, most of whom reside in the St. Louis metro and bi-state (Missouri and Illinois) areas. Given the longstanding nature of ADRC studies, many participants learn of these studies through word-of-mouth from a friend or family member. Other recruitment efforts include media appearances by ADRC staff and educational outreach efforts. Referral by a primary care physician or other health professional accounts for approximately 20% of participants.

Meta-analysis of the association between abnormal thyroid function status and the risk of dementia

• The study also showed that patients who were women were more likely to have low TSH levels and be overtreated.
• Senile plaques (SP) (diffuse and neuritic plaques), neuritic plaques (NP) and neurofibrillary tangles (NFT) were counted in five fields from the CA1 and subiculum of the hippocampus and five fields each from the four areas of neocortex.
• Most studies included individuals over 18 and under the age of 65, except for two studies where individuals were over 65 19,21.
• This was the sole criteria for defining and identifying thyroid disease as information concerning serum thyroid hormone levels was not available.
• With the increasing prevalence of thyroid dysfunction, it may be valuable for public health to focus on monitoring TSH concentrations.
• The dose was titrated until the suppression of TSH with the same proportion of dose adjustments in the placebo.

Dogs do not get sick from hantavirus, said Erin Phipps, a veterinarian with the New Mexico Health Department. The sheriff considers this an open investigation until they finish checking into cellphone data and receive results of the dog’s necropsy. Although there was no reliable way to determine the date and time when both died, all signs point to their deaths coming a week apart, Jarrell said.

Our results verified the findings of a meta-analysis conducted in 2016 after adding three new reports (6, 7, 8). The underlying processes of the relationship between hyperthyroidism and Alzheimer’s disease must be thoroughly studied. According to an autopsy in 2009, more neurofibrillary tangles and neocortical plaques were found in patients having higher total thyroxine levels (39). For the first time, Li, Yang etal. discovered in 2020 that patients with hyperthyroidism exhibited notably elevated levels of total serum tau in comparison to those with normal thyroid function (40).

The Association of Thyroid Disease with Risk of Dementia and Cognitive Impairment: A Systematic Review

The exact mechanisms for the connections between the two are inconclusive and need to be determined in future studies. Thyroid hormone acts as a neuromodulator and crucially impacts mood regulation, neurotransmitter function and regulation, brain development and function, neuroprotection and brain metabolism. The hippocampus displays a high concentration of receptors for TH and dysregulation of TH results in significant impairment of both cognitive and memory functions (65). Thyroid hormone enhances the action of nerve growth factor and promotes the growth of neurites (66).

• The presumed etiology of dementia is diagnosed based on standardized criteria (Morris et al., 2006).
• Clinical observations and experimental studies have indicated a relationship between thyroid hormones and AD or its pathology (9–12).
• Aghili et al. reported significant improvement in memory skills in the intervention group compared to the control group in a survey of 60 subclinical hypothyroid patients.
• These concurrent mechanisms may all be involved in the pathogenesis of Alzheimer’s disease (Figure 2).
• Therefore, it is vital to provide suitable therapy at the best time for each individual patient to prevent and treat cognitive deficits caused by thyroid dysfunction.
• We also know that patients with Alzheimer’s have low levels of T3 (2) (even within the normal range), indicating the importance of this hormone over other hormones such as Free T4.

Although we adjusted our risk estimate analyses for various comorbid diseases and medical conditions, in particular cardiovascular risk factors, to minimize the effect of comorbidity, other brain pathologies related to thyroid dysfunction may remain. In addition to cardiovascular disease, thyroid hormone dysregulation has been implicated in or is comorbid with hippocampal sclerosis, autoimmune diseases, and cerebrovascular disease, such as cerebral small vessel disease and stroke (38–41). Additional research controlling for these brain pathologies influencing thyroid function is required to elucidate the contribution of thyroid disease to AD.

These observations serve as a reminder that tau protein aggregation and phosphorylation are hallmarks of an AD pathological process that may be present in hyperthyroid patients. But unfortunately, in these studies, we were not able to find a causal relationship between high thyroid hormone levels and the development of AD. More importantly, plasma Tau levels only partially reflect the pathological process of AD and their diagnostic accuracy is poor compared to cerebrospinal fluid Tau levels (41). We look forward to finding more sensitive, specific and easily sampled biomarkers for AD in the future. Notably, our findings also demonstrated that there was a significant association with thyroiditis and AD.

Statistical Analysis

This decrease causes a block and delay in synaptic transmission, it also inhibits the proliferation and differentiation of neural stem cells (73). On another, the reduction in thyroid hormone makes neurons more sensitive to the neurotoxic effects of glutamate, which may be attributed to the ability of thyroid hormone in regulating extracellular levels of glutamate by modulating transporter proteins on astrocytes (74). Also, evidence from many studies has shown the importance of thyroid hormone supplementation combined with the use of cholinesterase inhibitors in reversing synaptic damage and restoring cognitive function (75, 78). Under normal conditions beta amyloid plaque is opsonized by the immune system and removed from the brain by microglia and monocytes (Travis, 1999).

When you take these hormones (medications), your body knows exactly what to do with them, it knows how to process them, and it knows how to eliminate them. They are operating under the standard conventional wisdom that thyroid status in the body can be measured adequately with the use of TSH and T4. I strongly believe so, and even the authors do suggest that the dose of thyroid hormone that you are taking may play a role. The authors are solely responsible for the design and conduct of this study, all study analyses, the drafting and editing of the manuscript, and its final contents.

6 Statistical analysis

To highlight the importance of T3 you need to have a basic understanding of how synthroid infants T3 functions in your body.