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Therapeutic potential of ADAM10 modulation in Alzheimer’s disease: a review of the current evidence
Alzheimer’s disease (AD), the most common neurodegenerative disease worldwide, is caused by loss of neurons and synapses in central nervous system. Several causes for neuronal death in AD have been introduced, the most important of which are extracellular amyloid β (Aβ) accumulation and aggregated t...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10012555/ https://www.ncbi.nlm.nih.gov/pubmed/36918870 http://dx.doi.org/10.1186/s12964-023-01072-w |
Sumario: | Alzheimer’s disease (AD), the most common neurodegenerative disease worldwide, is caused by loss of neurons and synapses in central nervous system. Several causes for neuronal death in AD have been introduced, the most important of which are extracellular amyloid β (Aβ) accumulation and aggregated tau proteins. Increasing evidence suggest that targeting the process of Aβ production to reduce its deposition can serve as a therapeutic option for AD management. In this regard, therapeutic interventions shown that a disintegrin and metalloproteinase domain-containing protein (ADAM) 10, involved in non-amyloidogenic pathway of amyloid precursor protein processing, is known to be a suitable candidate. Therefore, this review aims to examine the molecular properties of ADAM10, its role in AD, and introduce it as a therapeutic target to reduce the progression of the disease. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01072-w. |
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