The role of the basal forebrain in the pathogenesis of Alzheimer’s disease

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by impaired cognitive functions, from minor deviations to dementia, as well as altered behavior. Typical features of this disease include the presence of senile plaques, neurofibrillary tangles, synaptic damage, and neuronal loss. Many factors contribute to cognitive decline in patients with AD. According to the cholinergic hypothesis, which prevailed at the end of the last century and remains relevant today, a key event in the pathogenesis of AD is the loss of cholinergic neurons in the basal forebrain (BFB), found in this region in AD patients. However, the death of neurons deprives the brain of a range of other neurochemical agents. In addition, the occurrence of AD may also be caused also caused by other morphofunctional abnormalities in this area of the brain. In modern literature there is no summary information about the role of BFB in the pathogenesis of AD. The functions of the BFB and the mechanisms of regulation of the neural network of this part of the brain in normal conditions and in neuropathologies remain unclear. This review comprehensively examines the involvement of the BFB and its connections with other brain regions in the development of AD. The article includes data from clinical observations and experiments conducted both on healthy animals and on those with models of this disease. The analysis of the available literature data will improve the understanding of the functioning of the BFB normally and its disturbances during the development of AD, which can advance the development of therapeutic approaches for the treatment of this disease.