Therapy and diagnosis of Alzheimer’s disease: from discrete metal complexes to metal–organic frameworks
Metadatos
Mostrar el registro completo del ítemEditorial
Royal Society of Chemistry
Fecha
2023-06-08Referencia bibliográfica
J. Mater. Chem. B, 2023, 11, 7024[DOI: 10.1039/d3tb00427a]
Patrocinador
MOFSEIDON project (PID2019- 104228RB-100, MCI/AEI/FEDER); AgroMOFs project (TED2021-132440B-I00); MCIN/AEI/10.13039/50110 0011033; NextGenerationEU/PRTR; Margarita Salas contract 401; Ministerio de Universidades and Next Generation; B- FQM-394, ProyExcel_00105; ProyExcel_00386; Consejería de Universidad, Investigación e Innovación de la Junta de Andalucía; Grant (RYC2021-032522-I); MCIN/AEI/10.13039/ 501100011033Resumen
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 b-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: Ab peptides, hyperphosphorylated tau proteins, synaptic
dysfunction, and mitochondrial failure with subsequent oxidative stress





