The Association Between Thyroid Diseases and Alzheimers Disease in a National Health Screening Cohort in Korea

Also, the expression of NMDAR subunit GRIN2B gene is downregulated in the hippocampus tissue, which affects spatial memory that depends on the hippocampus (55). Moreover, hyperthyroidism has been found to potentially result in a decline in brain-derived neurotrophic factor (BDNF) levels (56). As a result, patients with hyperthyroidism may face difficulties in learning tasks that heavily rely on the hippocampus and are prone to forgetting them at a faster rate. Additionally, as TRH levels drop, the MAPK pathway’s signal weakens, releasing its inhibition on GSK3-activity and causing tau to become hyperphosphorylated (57).

The analytical sample for the autopsy study is 143, only five of whom had high and four of whom had low thyrotropin levels.
Moreover, it is crucial to prioritize early detection, diagnosis, and treatment by assessing thyroid function in individuals at a high risk of developing neurodegenerative diseases.
Also, while the study was not designed to assess whether treating thyroid dysfunction would improve brain function, the authors felt that it was unlikely to help, particularly in those with subclinical thyroid disease.
Five other studies (9, 12, 15, 22, 23) were not included in the meta-analysis or dose–response meta-analysis owing to irrelevant data.
In the experience of dementia specialist Suzanne Schindler, MD, that’s what patients in the early stages of Alzheimer’s disease so often want.
In the lecanemab trial, patients on the drug had a slightly slower decline in memory, thinking skills, and day-to-day functioning than patients given the placebo.

A standardized difference of ≤0.1 was deemed an ideal balance, and a standardized difference of ≤0.2 was treated as acceptable balance. Statistical analysis was conducted by using SAS ver. 9.4 (SAS Institute Inc., Cary, NC, USA). All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The best way to ensure that you live a long and healthy life is by looking at more than just your thyroid.

Meanwhile, the impact of cardiovascular disease on AD can be explained by the “two-hit hypothesis”, namely reduced cellular blood flow and blood-brain barrier dysfunction (64). These two events have a synergistic role in the accumulation of βA in the brain, which leads to neuronal loss and cognitive decline. Alzheimer’s disease (AD), often colloquially referred to as late-onset dementia, is a gradually advancing degenerative disorder that specifically targets the CNS. The biological processes underlying neurodegeneration in Alzheimer’s disease are still hugely controversial, including other protein components that co-aggregate with βA, loss of synaptic homeostasis, clearance of damaged proteins, and network connectivity in the cortex (8, 9).

Characteristics of Participants

Other studies have found no significant association between any type of thyroid dysfunction and DAT onset (Lindeman et al., 1999; Luboshitzky et al., 1996; van der Cammen et al., 2003). Given this lack of consensus, the impact of thyroid disease and thyroid hormone replacement therapy on AD risk is unclear. If thyroid disorder, or the use of thyroid medications, is related to developing DAT, it would support the idea of an underlying link between these diseases.

Sensitivity analysis

According to the 2010 US Census data, the overall prevalence of AD was estimated to be 14.5% and the annual incidence was 2.3% (4). Pathologically, this disease is known to be attributed to extracellular amyloid deposition and intracellular neurofibrillary tangles of hyperphosphorylated tau (5). However, the causes of these features and those of the disease have not yet been elucidated.

A lack of attention, abstraction capability, and problem-solving ability can occur during the illness. A lack of diagnosis can lead to severe cognitive deficits and dementia that can become lifelong if not treated 14. The severity of cognitive impairment remains unknown, although there has been proven evidence of cognitive dysfunction in hypothyroidism. As shown above, the impact of hypothyroidism on AD can be examined through various mechanisms, including diminished neuromodulation, alterations in gene expression, impaired autophagy, elevated oxidative stress, and cerebral metabolic dysfunctions (Figure3). It should be noted that these elements do not operate independently, but instead collaborate synergistically to foster the onset and advancement of AD. And we must point out that these are only possible mechanisms for the link between hypothyroidism and Alzheimer’s disease.

How To Lose Weight Rapidly If You Have Hypothyroidism

We require longer-term, large-scale clinical trials and more in-depth basic research at various levels, including molecular, cellular, and animal models. We look forward to more in-depth studies in the future to gradually improve the pathological mechanisms between thyroid dysfunction and Alzheimer’s disease, and to find a more comprehensive and convincing network of mechanisms. Moreover, it is crucial to prioritize early detection, diagnosis, and treatment by assessing thyroid function in individuals at a high risk of developing neurodegenerative diseases.

For the first time, Li, Yang et al. discovered in 2020 that patients with hyperthyroidism exhibited notably elevated levels of total serum tau in comparison to those with normal thyroid function (40).
I’ve already mentioned previously that hypothyroidism is a potentially reversible cause of dementia and when you stop taking your thyroid medication you are putting yourself into a state of hypothyroidism.
This approach could significantly contribute to the prevention and deceleration of Alzheimer’s disease progression.
After a 12-month trial on an older population, Stott et al. observed no effect on executive function as measured by Letter Digit Coding Test.
More critically, maintaining homeostasis of thyroid hormone levels within the brain is critical to the proper functioning of the CNS, and even relatively minor deviations in brain hormone levels can cause severe behavioral and cognitive impairment (106).

This was the sole criteria for defining and identifying thyroid disease as information concerning serum thyroid hormone levels was not available. Use of thyroid hormone replacement therapy at the baseline assessment was ascertained, and was defined as any form of exogenous T3 or T4 and included all forms of levothyroxine and liothyronine of both synthetic and natural origin. Overall, the risk from mild hypothyroidism appears to be low and most relevant in combination with other risk factors 10; 12.

Signs of Low Collagen In Hypothyroid Patients

During the study, some of the patients taking supplemental thyroid hormone medication had low TSH levels. In the follow-up period, 7.2% (4,779) of patients who were taking an excessively high dose of levothyroxine got a new cognitive disorder diagnosis. APP serves as the predecessor of beta amyloid fragments that aggregate to form plaques found in the brains of patients with AD. Thyroid hormones have the ability to regulate the production of different APP isoforms (Latasa et al., 1998).

Several processes, such as obesity, leptin resistance, inflammation, chronic illness, prescription medications (and so on), limit how well your body can turn T4 into T3. Both free T4 and free T3 are created and produced by your thyroid gland, but most of the free T3 in your bloodstream comes from the conversion of T4 into T3. This synthroid portugal is important because hyperthyroidism is another well-documented cause of early-onset dementia (Alzheimer’s type) (3). It is also possible that some people are receiving too much medication (those with an extremely suppressed TSH) which may also cause further confusion among patients who are being overdosed. This link has caused some people to believe that it is actually the medication itself that is causing dementia. FT3, free triiodothyronine; FT4, free thyroxine; NOS, score of Newcastle–Ottawa Scale; TSH, thyroid-stimulating hormone.