According to recent research, the primary cause of the disease is represented by an increase in the production of ß-amyloid polypeptides. They then gradual polymerize and form amyloid plaques that are characteristic histopathologic feature of this disease. The cause of increased production of ß‑amyloid is known only for familial forms of the disease, but these represent only a tiny fraction (1–2 %).  The presence of apolipoprotein E4 (ApoE4) is the most prevalent genetic risk factor of Alzheimer’s disease. We study the cellular and molecular mechanisms underlying the neuronal and synaptic effects of apoE4 and their neuronal specificity since one of the characteristics of the disease is the damage to the cholinergic neurons.

Furthermore, we try to clarify processes underlying disorders of cognitive functions (e.g. memory, space orientation, and learning) that accompany Alzheimer’s disease.