Thyroid hormones action on 3xTg-AD (APPswe, PS1m146v, tauP301L) Alzheimer's Disease mice model

Abstract

The prevalence of brain disorders affecting cognition (such as stroke and dementia) increases steadily in a linear fashion as age increases. Alzheimer's disease (AD) is the most frequent cause of dementia, increasing in prevalence from less than 1% below the age of 60 years to more than 40% above 85 years old. Worldwide, 35.6 million people have either Alzheimer's or dementia, according to the World Health Organization; it is expected to triple by 2050. The neuropathologic features of this disease are senile plaques and neurofibrillary tangles, which are present in memory structures and cerebral cortex. Several population-based studies have demonstrated an association between hypo-or hyperthyroidism and dementia in the last two decades. Patients with AD as well as other dementias had signs of mild brain hypothyroidism. This neurodegenerative disease represent a challenge for basic science and clinical medicine because of increasing prevalence, social cost, complex biochemistry and pathology, and lack of mechanism-based treatments. This study focuses on evaluation of possible mechanisms of thyroid hormones lack and administration in the management of neurological changes accompanied with AD on 3xTg-AD (APPswe, PS1m146v, tauP301L) Alzheimer's Disease mice and model and wild type animals. (AU)