Therapy and diagnosis of Alzheimer's disease: from discrete metal complexes to metal-organic frameworks

Alzheimer's disease (AD) is a neurodegenerative disorder affecting 44 million people worldwide. Although many issues (pathogenesis, genetics, clinical features, and pathological aspects) are still unknown, this disease is characterized by noticeable hallmarks such as the formation of & beta;-amyloid plaques, hyperphosphorylation of tau proteins, the overproduction of reactive oxygen species, and the reduction of acetylcholine levels. There is still no cure for AD and the current treatments are aimed at regulating the cholinesterase levels, attenuating symptoms temporarily rather than preventing the AD progression. In this context, coordination compounds are regarded as a promissing tool in AD treatment and/or diagnosis. Coordination compounds (discrete or polymeric) possess several features that make them an interesting option for developing new drugs for AD (good biocompatibility, porosity, synergetic effects of ligand-metal, fluorescence, particle size, homogeneity, monodispersity, etc.). This review discusses the recent progress in the development of novel discrete metal complexes and metal-organic frameworks (MOFs) for the treatment, diagnosis and theragnosis of AD. These advanced therapies for AD treatment are organized according to the target: A & beta; peptides, hyperphosphorylated tau proteins, synaptic dysfunction, and mitochondrial failure with subsequent oxidative stress.

Automated summary

Alzheimer's disease is a neurodegenerative disorder characterized by β-amyloid plaques, tau protein hyperphosphorylation, reactive oxygen species overproduction, and reduced acetylcholine levels. Current treatments aim at regulating cholinesterase levels, but there is no cure. Coordination compounds show promise in AD treatment and diagnosis due to their unique features. This review discusses the development of novel metal complexes and metal-organic frameworks for AD treatment targeting β peptides, hyperphosphorylated tau proteins, synaptic dysfunction, and oxidative stress caused by mitochondrial failure.