No abstract

Alzheimer’s disease (AD) described as a chronic and irreversible neurodegenerative disease remains the most common cause of dementia. Due to the aging of the population, the incurability of AD has become a growing problem of medicine in the 21stcentury. Current treatment is only symptomatic, providing minimal, temporary improvement in the patient’s cognitive function. This paper presents the latest trends in the search for effective pharmacotherapy capable of preventing or inhibiting AD progression. Since the exact pathogenesis of Alzheimer’s disease is not known, the main therapeutic strategies are based only on the following hypotheses: amyloid cascade, tau protein, oxidative stress, neuroinflammation and those associated with dysfunction of the cholinergic system as well as glutamatergic. Most of the compounds currently tested in clinical trials are targeted at pathological amyloid β (A β), which is considered the cause of neurodegeneration, according to the most widely described cascade theory. Most of the compounds currently tested in clinical trials are targeted at pathological amyloid β (Aβ), which is the main cause of neurodegeneration according to the widely described theory of the amyloid cascade. Attempts to fight the toxic Aβ are based on the following: immunotherapy (vaccines, monoclonal antibodies), compounds that inhibit its formation: γ-secretase inhibitors/modulators and β-secretase. Immunotherapy can also be us,ed to increase the clearance of hyperphosphorylated tau protein, the occurrence of which is another feature of Alzheimer’s disease. In addition to immunotherapy, anti-inflammatory, metabolic and neuroprotective compounds have been the subject of a number of studies. A range of symptomatic compounds that improve cognitive functions by compensating cholinergic, noradrenergic and glutamatergic signaling deficits have also been investigated in clinical trials.