In recent years, accumulated evidence suggests the involvement of the LRP1 protein in the pathogenesis of Alzheimer's disease (AD), the most common primary cause of dementia syndrome. The LRP1 protein is a member of the LDL receptor family with multiple roles, of which the potentially most important is the mediation of cholesterol entry into cells, especially neurons, and many other roles are related to the metabolism of the amyloid precursor protein (APP), whereas some relate to tau protein signaling pathways. Therefore, the purpose of this research was to examine the expression levels of LRP1 protein in the hippocampus of persons who suffered from AD and persons who died due to other causes and did not have neurological or psychiatric disorders, i.e. whether increased or decreased expression of LRP1 protein is associated with neuropathological changes characteristic of AD, especially with neurofibrillary degeneration. The results of the analysis of six postmortem tissue samples of the hippocampus (three from persons with AD and three from persons who died of non-neurological causes) were obtained by the simultaneous visualization of LRP1 protein and tau protein phosphorylated on the Ser202/Thr205 epitope using the AT8 antibody showed increased LRP1 protein levels in AD patients compared to control samples. The greater levels of neurofibrillary changes assessed by neuronal AT8-immunoreactivity negatively correlated with the LRP1 protein expression levels. This preliminary result confirms the initial hypothesis on the involvement of the LRP1 protein in the development of AD, but for a firmer conclusion, it would be necessary to analyze a much larger number of samples in different stages of the disease.