Heavy metals are reported as neurodegenerative disorders progenitor. They play a role in the abnormal amyloid beta 40 (Aβ40) protein concentrations, the main hallmarks of Alzheimer's disease (AD). The aim of the present work is to study the morphological ultrastructural changes by transmission electron microscopy and measurements of Aluminium and Aβ40 protein concentration in rats’ hippocampus due to Alzheimer's-like disease in rats. Fifty male Albino Wistar rats were divided into five groups; the first group acted as the control group, while the other four groups each received 100 mg/kg of aluminium chloride (AlCl3) over the course of 2, 4, 6, and 8 weeks. The results indicated significant increase (p˂0.05) of alumininm and significant decrease (p˂0.05) of Aβ40 in the hippocampus of rats due to AlCl3 administration starting from 2 and 6 weeks, respectivily. Histological ultrastructural hippocampus changes were observed starting from 2 weeks of AlCl3 administration to reach the most damaged structure after 8 weeks, where its nucleus appeared shrunken with a condensed chromatin beside marked loss of the cytoplasmic organelles including mitochondria, rER, and Golgi apparatus. Also, vacuolation was clearly observed at the remnants of cytoplasm. According to the results of the current investigation, there is a significant link between multiple exposure to environmental heavy metals and the pathophysiology of AD by altering Aβ 40, which causes neuronal death, as well as histological and ultrastructural changes in the rat hippocampus.