Cognitive and Memory Decline in Thyroid Disorders: A Biomarker Based Cross Sectional Study in Aging Adults

The pathophysiology of Alzheimer's disease (AD) involves a complex interplay of several factors like oxidative stress, hypercalcemia, decreased acetylcholine, which may act independently or synergistically to drive cognitive decline. The accumulation of Aβ42 fragments derived from amyloid precursor protein is hall mark of AD. Epidemiologic studies suggest that thyroid dysfunction may increase the risk of early-onset AD. This study aims to provide the potential mechanisms linking thyroid dysfunction and AD, both common in older adults by evaluating serum memory and cognitive biomarkers in aging patients with thyroid disorders.

Serum levels of Aβ42, acetylcholinesterase (AChE), brain-derived neurotrophic factor (BDNF), GSH, and calcium were measured in 45 patients each with hyperthyroidism and hypothyroidism, and compared with 30 age- and sex-matched healthy controls. Serum Aβ42 and BDNF were quantified using sandwich ELISA. AChE, GSH, and calcium were measured spectrophotometrically.

Aβ42 levels were significantly elevated in both hyperthyroid (p=0.000) and hypothyroid patients (p=0.043) compared to controls.BDNF and AChE levels were significantly elevated in both thyroid disorder groups versus healthy individuals (p=0.000).These elevations were relatively more pronounced in hypothyroid patients compared to hyperthyroid patients (BDNF: p=0.036; AChE: p=0.034). Serum calcium levels were significantly increased in both hyperthyroid and hypothyroid patients compared to controls (p=0.000). GSH levels were significantly elevated in hyperthyroid patients compared to both hypothyroid patients and healthy controls (p=0.000).

Elevated Aβ42, AChE, and calcium levels may contribute to persistent cognitive and memory impairment in thyroid disorders, underscoring the need to evaluate memory markers to reduce the risk of dementia.