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.
Drug Development for Alzheimer’s Disease: Microglia Induced Neuroinflammation as a Target?