It is estimated that Alzheimer’s disease (AD) affects
tens of millions of people, comprising not only suffering patients, but also their relatives and caregivers. AD is one of age-related
neurodegenerative diseases (
NDs) characterized by progressive synaptic damage and neuronal loss, which result in gradual
cognitive impairment leading to
dementia. The cause of AD remains still unresolved, despite being studied for more than a century. The hallmark pathological features of this disease are
senile plaques within patients’ brain composed of
amyloid beta (Aβ) and neurofibrillary tangles (NFTs) of
Tau protein. However, the roles of Aβ and Tau in AD pathology are being questioned and other causes of AD are postulated. One of the most interesting theories proposed is the causative role of
amyloid β oligomers (AβOs) aggregation in the pathogenesis of AD. Moreover, binding of AβOs to cell membranes is probably mediated by certain
proteins on the neuronal cell surface acting as AβO receptors. The aim of our paper is to describe alternative hypotheses of AD etiology, including genetic alterations and the role of misfolded
proteins, especially Aβ oligomers, in Alzheimer’s disease. Furthermore, in this review we present various putative cellular AβO receptors related to toxic activity of oligomers.