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The Association of Thyroid Disease with Risk of Dementia and Cognitive Impairment: A Systematic Review
Samples were evaluated by one of three neuropathologists who were blinded to clinical information. 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. Fields were selected for counting from areas with the highest numbers of lesions, and the field with the highest count was taken to represent the cortical or hippocampal area.
Recent national reports on the epidemiology of thyroid dysfunction state that approximately 4.5% of Americans are affected (CDC, 2006). The National Center for Health Statistics reports that 2.2% of the American population utilizes prescription thyroid medications (CDC, 1998). Recent research shows that the prevalence of thyroid dysfunction increases with age (Hollowell, 2002), and therefore, one would expect a larger proportion of individuals in our sample, comprised of older adults, to have thyroid dysfunction. The Colorado Thyroid Disease Prevalence Study reported thyroid disease and medication usage rates at 11.7% and 5.9%, respectively (Gay, 2000). Although the N for that study was larger, the study population was similar to ours in that participants were older, more educated, and larger proportions were Caucasian and female compared to the general population of the area (Gay, 2000). Participants who reported either ongoing or previous thyroid dysfunction at the baseline assessment were identified.
Thyroid function and Alzheimer’s disease
Mild memory and thinking problems can have numerous causes other than Alzheimer’s, Dr. Schindler explains—and sometimes it’s as simple as medication side effects or a treatable health condition, like sleep apnea or a thyroid disorder. Then, if they suspect Alzheimer’s, they’ll order a PET scan or a lumbar puncture to look for amyloid buildup. Participants who received treatment with levothyroxine for more than 3 months or who had goiter, hypothyroidism, thyroiditis, or hyperthyroidism were evaluated as described previously (17), and these conditions were included as independent variables. Participants with AD, which was used as the dependent variable in our analysis, were assessed and included as reported in our previous work (18). The authors examined data from 74, 565 people participating in 23 different clinical trials whose thyroid hormone levels had been measured (57.5% women and 42.5% men). But the researchers think the findings add to a growing body of evidence that there could be cognitive risks for older adults who are taking thyroid medication—and who may not even need to be taking it.
- Stopping your thyroid medication will cause hypothyroidism which may only further increase your risk of dementia.
- However, it has also been suggested that TTR was not necessary for the upkeep of thyroid hormone homeostasis (34).
- In recent years, many studies have highlighted the significance of antithyroid therapy in enhancing cognitive function.
- In the dose–response meta-analysis, studies with at least three categories of TSH concentrations and the number of dementia cases presented, according to the different categories of TSH concentrations, were retained.
- As the pathogenic process of AD worsens, there is a continuous accumulation of toxic βA.
The Best Fat Burners For Hypothyroid Patients
The effect of thyroid dysfunction on AD includes neuron death, impaired synaptic plasticity and memory, misfolded protein deposition, oxidative stress, and diffuse and global neurochemical disturbances. Conversely, AD can also contribute to thyroid dysfunction by affecting the stress repair response and disrupting pathways involved in thyroid hormone (TH) production, transport, and activation. Furthermore, this review briefly discusses the role and significance of utilizing the thyroid as a therapeutic target for cognitive recovery in AD.
The available drugs for Alzheimer’s could only temporarily ease some symptoms—not change anything about the underlying brain disease. But in just the past year and a half, two anti-amyloid drugs—lecanemab (Leqembi) and donanemab (Kisunla)—that can slow the progression of early Alzheimer’s disease have been approved in the US. JK and HL participated in the interpretation of the data and drafted and revised the manuscript. HC designed the study, participated in data collection and data interpretation, and revised the manuscript.
Sounds scary (and it can be), but ARIA most often causes no symptoms and goes away on its own, Dr. Schindler says. However, in some cases, it can lead to problems like headaches, dizziness, or nausea, and there is about a 1% chance of it causing potentially fatal brain bleeding or swelling. That said, people shouldn’t start anti-amyloid treatment if they have certain medical conditions or are taking medications that boost their odds of serious bleeding. Patients with newly confirmed hypothyroidism were included in three studies 16-18.
- Since neuronal and astroglial cells are targets of thyroid hormone, lack of this hormone may create an environment unable to support development, differentiation, and survival of microglial cells due to a lack of growth factor secretion from developing neurons and astrocytes.
- This thesis is supported by Mallet, et al. (2002) who found microglial processes to be promoted by the presence of T3 in vitro.
- GABA inhibits the release of TSH from the pituitary gland, while thyroid hormones affect multiple components of the GABA system.
- Two investigators independently identified eligible studies, screened title/abstract, and extracted data.
Inadequate Treatment or Negative Side Effects?
A Cox proportional hazards regression delayed entry model with age as the time scale was used to calculate hazard ratios (HR) with 95% confidence intervals (95% CI) for total dementia and AD (with and without cerebrovascular disease). Age of onset was assigned as the midpoint of the interval between the last examination without dementia and the first follow-up examination with dementia. Subjects who died or did not participate in subsequent follow-up examinations were censored as of the time of their last evaluation. Cox models are typically used when the synthroid consecuencias time-to-event is measured continuously across participants. Because it is difficult to surveil and dementia onset is usually gradual, the mid-way point between two visits is typically used as a measure of time of onset.
Instead, it is much more likely that an inadequate treatment with thyroid hormone, causing low thyroid status in the body, contributes to dementia and not long-term use of the medication itself. Procedures for autopsy and neuropathological examination have been described elsewhere 24. After fixation, brains were weighed, the cerebellum and brainstem were removed from the cerebral hemispheres, and all were cut serially in the coronal plane at 1-cm thickness. Slices were examined for grossly apparent neuropathologic lesions, and the whole brain and slices were photographed. Tissue from four areas of neocortex (middle frontal gyrus, inferior parietal lobule, middle temporal gyrus, and occipital cortex) and two areas of hippocampus (CA1 and subiculum) was used to prepare Bielschowsky silver-stained sections.
We investigated the associations between several thyroid diseases and AD in a nested case-control study. A deeper dive into the biology of thyroid hormone helps explain both why hypothyroidism poses a risk for dementia and why thyroid hormone replacement is ineffective in reducing that risk for many people. Although hypothyroid-related cognitive impairment is considered reversible, the response to thyroid hormone replacement therapy is variable and often incomplete 3.
Studies with moderate to low risk of bias were evaluated using their respective quality check tools. According to these studies, the plausible rationale behind the reversal of memory with LT-4 treatment is restoring thyroid-stimulating hormone (TSH), thyroxine (T4) levels, and gamma-aminobutyric acid (GABA) concentrations. People with abnormal thyroid function should be screened for cognitive dysfunction using specific neurocognitive tests and start treatment with LT-4 regardless of symptom presentation. Multi-dose randomized placebo-controlled intervention studies are recommended to assess the effect of LT-4 on lowering the risk of dementia in hypothyroid patients. After the link between clinical thyroid dysfunction and cognitive abnormalities was first described by Asher as “myxoedematous madness” in 1949 (6), interest in the association between thyroid disorders and dementia increased.