Hypocholesterolemia is a risk factor for neurodegenerative diseases that impairs neuronal function and reduces the neurogenesis. In light of its association with neurodegenerative disease, the current investigation set out to clarify how elevated cholesterol levels could impact oxidant and antioxidant, which necessitated the importance of studying the histopathological changes in the nervous tissue of the central system that resulting from excess dietary fats. Twenty adult albino male rats weighing 178-200 grams were included in this study. Animals were randomly divided into two equal groups with 10 rats each group. Control group was fed on regular normal diet, while the treated groups were received the addition of 1% cholesterol in their food for the period of 28 days. Examination of the neurological sections revealed that the pattern of disruption of nerve tissue cells with varying degrees of deposition of neurofibrillary tangles on nerve cells, manifested by intracellular and extracellular deposition of beta-amyloid plaques of the central nervous system, which permeate cerebral layers and are less permeable than in the cerebellum and spinal cord parts. As it turns out, neuronal atrophy nuclei with neuroglia proliferation and inflammatory infiltration cells of neural tissues. In conclusion, our results indicated that hypercholesteremia had a negative impact. Elevated levels of oxidative stress lead to damage to the biochemical structural integrity of neurons and Glial cells in the cerebral cortex in a significant way, the restoration of which is often fundamental in neurodegenerative diseases.