Alzheimer’s disease: Pathogenesis, diagnosis, and therapeutic strategies

Abstract

Presence of Alzheimer's disease (AD) is one of the main causes of progressive dementia. The pathophysiology of AD, a neurodegenerative disease, has been linked to intracellular neurofibrillary tangles composed of hyperphosphorylated τ-protein and extracellular aggregation of amyloid β (Aβ) plaques in the cortical and limbic regions of the human brain. Memory loss and increasing neurocognitive impairment are its hallmarks. Senile plaques are formed when Aβ40 and Aβ42 monomers are produced as a result of the aberrant processing of APP by β- and γ-secretases. These monomers then oligomerize and aggregate. Additionally, infectious infections such as HIV exacerbate the condition. Furthermore, microglial infiltration is triggered during disease pathogenesis by high quantities of Aβ peptides in the central nervous system. When microglia come into contact with Aβ, they become activated, endocytose Aβ, and help to remove them through TREM2 surface receptors, all the while inducing an innate immune response to the aggregation. The current review covers the state of the art in AD therapies and diagnostics, including labeling and imaging techniques used as contrast agents for enhanced vision and sensing of the plaques. It also provides a full report on the causative elements leading to AD. The analysis highlights the critical need for nanotechnology as a successful therapeutic approach to boost medication bioavailability in the central nervous system.