New therapeutic strategies for Alzheimer’s disease

Abstract

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