Adela Elena Joanta, Oana Persa, Remus Moldovan, Nicoleta Decea and Adriana Muresan
Accepted Abstracts: J Neurol Neurophysiol
Alzheimer disease is the most common neurodegenerative disease among the elderly. Common pathological hallmarks which manifest in Alzheimer disease include senile plaques of amyloid-β aggregates and neurofibrillary tangles comprising of paired helical filaments of tau protein. Other irregularities include neuronal and dendritic loss, accumulation of neuropil threads and dystrophic neurites, and atrophy of the brain. While they are useful in diagnosing AD, pathological hallmarks do not provide insight towards understanding the pathogenesis of the disease. Also, the oxidative imbalance is one of the earliest manifestations of Alzheimer disease actually preceding the classic pathology of amyloid β deposits and neurofibrillary tangles. On the other hand, thyroid dysfunction is associated with cognitive impairment and dementia, including Alzheimer disease. It remains unclear whether thyroid dysfunction results from, or contributes to Alzheimer pathology. White Wistar rats were injected intra-hippocampally aggregated amyloid β-peptide to produce Alzheimer?s disease model. The hyperthyroidism was induced in Alzheimer rendered rats by intraperitoneally administration of thyroxine using a low dose and a high dose, daily for 14 days, while the hypothyroidism was induced by daily oral administration of propylthiouracil (0.05%) for 14 days. We investigated the thyroid hormone involvement on cognitive impairment, cholinergic function and on prooxidant/antioxidant balance in Alzheimer?s disease model. This research study aimed to examine the feasibility of using thyroid hormone as a therapeutic agent for Alzheimer?s disease.
Alzheimer disease is the most common neurodegenerative disease among the elderly. Common pathological hallmarks which manifest in Alzheimer disease include senile plaques of amyloid-β aggregates and neurofibrillary tangles comprising of paired helical filaments of tau protein. Other irregularities include neuronal and dendritic loss, accumulation of neuropil threads and dystrophic neurites, and atrophy of the brain. While they are useful in diagnosing AD, pathological hallmarks do not provide insight towards understanding the pathogenesis of the disease. Also, the oxidative imbalance is one of the earliest manifestations of Alzheimer disease actually preceding the classic pathology of amyloid β deposits and neurofibrillary tangles. On the other hand, thyroid dysfunction is associated with cognitive impairment and dementia, including Alzheimer disease. It remains unclear whether thyroid dysfunction results from, or contributes to Alzheimer pathology. White Wistar rats were injected intra-hippocampally aggregated amyloid β-peptide to produce Alzheimer?s disease model. The hyperthyroidism was induced in Alzheimer rendered rats by intraperitoneally administration of thyroxine using a low dose and a high dose, daily for 14 days, while the hypothyroidism was induced by daily oral administration of propylthiouracil (0.05%) for 14 days. We investigated the thyroid hormone involvement on cognitive impairment, cholinergic function and on prooxidant/antioxidant balance in Alzheimer?s disease model. This research study aimed to examine the feasibility of using thyroid hormone as a therapeutic agent for Alzheimer?s disease.
