Yüksek doz 25 hidroksi kolekalsiferolün farelerde skopolamin ile oluşturulan alzheimer tipi demans modelinde hipokampüs ve serebral korteks bölgesine etkisinin histopatholojik olarak değerlendirilmesi

This study was designed to understand and investigate how 25 hydroxy calciferol (vitamin D) induces Alzheimer's-type dementia in mice, and how dementia has a positive or negative effect on the formula. Alzheimer's is a global health problem. An irreversible and progressive neurodegenerative management of Alzheimer's disease. Cognitive changes are receptors with cerebral atrophy neurons veal loss and neuropathological effects involving misfolded and aggregated cells of β-amyloid peptides (Aβ) and tau proteins. Two main pathological structures are depending on the disease. These are amyloid plaques that accumulate outside the cell and neurofibrillary tangles that form inside the cell. These proteins, which accumulate inside and outside the cell, impair axonal transport, interneuron observers, and neurotrophic factor, envelop intracellular shields and increase oxidative stress. Twenty c57bl/6 male mice with a body weight of 20-25 g were used in this study. Vitamin D tests were done. Accordingly, investigate the underlying causes of AD and. The development of treatments that will change the course of the illness becomes even more important. Diagnostic criteria were established in the years when biomarkers for AD diagnosis, patient anamnesis, clinical examination, neuropsychological tests and differential diagnosis were not available. Neurotrophin production of some protective vitamin D, which has been made in recent years, stimulates neuronal shield shelter by affecting the spread of shield channels and prevents oxidative stress by regulating some detoxification steps. And in this way, it is observed that it can exert a protective effect on neurons. Vitamin D is formed as a group of stars that are soluble in fat and organic solvents but insoluble in water. Until now, it was not discussed whether it should be evaluated as a hormone or a vitamin. However, it is studied as a prohormone by researchers because it reaches organs and tissues through its archives and undertakes important points. We aimed to examine the morphological changes of vitamin d in the hippocampus and cerebral cortex in the Alzheimer's fee model by histological analysis, and our guess is that we aim to have a protected area of vitamin d in this model. VDR is known to occur in large areas of the brain such as the cerebellum, hypothalamus, basal nodes and hippocampus. It has been suggested that vitamin D's effect on neuronal cell death and functionality may be shown by decreasing the expression of L-type calcium channels or increasing the level of VDR in order to facilitate the recovery of neurons or to facilitate the turn back of the brain to its previous function after neuron detriment. Premised on this, we think of that high-dose vitamin D increases the VDR level in the hippocampus and can act against neurodegenerative processes, and has a neuroprotective effect on the elimination of amyloid plaques, which is the most important pathology of Alzheimer's disease.The H-score was calculated on iNOS Amyloid-Beta immunohistochemistry staining, and there was a significant difference between the results of the scopolamine and control groups. Amyloid-Beta immunohistochemistry staining showed intense amyloid plaque formation of scopolamine cells and was rare in the test instruments. Key words: Alzheimer's Disease, Vitamin D, Scopolamine, Dementia, Amyloid plaques