Introduction: This study investigated the influence of chronic stress on changes in Fe metabolism. Disturbed homeostasis Fe and increased amount of Fe were observed in many neurodegenerative diseases. The accumulated excess of Fe causes oxidative damage, amyloid accumulation and neurodegeneration. Goals: To make immunochemical and histological coloring on Fe and amyloid from the brain tissue of young and old Sprague Dawley rats, and to determine the possible association of chronic stress, metabolic disorders of Fe and neurodegeneration. Materials and Methods: 40 females of Sprague Dawley rats were divided into 4 groups: 1. young animals exposed to fake stress, 2. young animals exposed to chronic stress, 3. old animals exposed to fake stress, 4. old animals exposed to the chronic stress. The research is structured as a study of pairs. In order to prove the presence of Fe in brain sections we used the modified Perls-DAB method. By the immunohistochemical method, with the help of antibodies to transferin and tau protein, and the corresponding secondary antibodies visualized with diaminobenzidine, we showed the position of the transferrin receptor and intracellular proteins precipitates. We visualized the amyloid with the histological coloring of Congo Red. Results: The key findings are that aging in animals increases the accumulation of Fe in the brain, on the other hand, chronic stress lowers the level of Fe, both in young and older groups. Expression of the transferrin receptor follows the same pattern as the accumulation of Fe. SNR nucleus cells are not prone to accumulation of pTAU. Just as with pTAU, we did not prove that aging or stress leads to an increase in the number of senile plaques. Conclusion: The hypothesis was not confirmed, chronic stress did not cause the accumulation of Fe in SNR neurons in neither young nor older female rats.