Alzheimer’s disease, amyloid-β peptides and ubiquitin-proteasome system: Therapeutic perspectives

What is it about?

The Alzheimer’s disease – an age-related neurodegenerative disorder leading to a progressive cognitive impairment – is characterized by an intracerebral accumulation of soluble β-amyloid (Aβ) oligomers, followed by the appearance of abnormally ubiquitinylated neurofibrillary tangles – a process associated with a chronic inflammation. The systematic presence of ubiquitinylated inclusions reflects a decrease in the proteasome activity due to (and contributing to) the presence of Aβ oligomers – a central dysfunction in the etiology of the disease. The involvement of the ubiquitin-proteasome system opens new therapeutic perspectives for both prevention and treatment.

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Why is it important?

Understanding the molecular and cellular mechanisms involved in the development of Alzheimer's disease and developing appropriate intervention strategies are the basis of innovative therapeutic approaches. The involvement of the ubiquitin-proteasome system in the pathophysiological process of Alzheimer's disease offers new possibilities for therapeutic intervention. Combined treatment strategies, combining immunoproteasome inhibitors, proteasome activators and modulators of β-amyloid peptide aggregation could prove useful in the future to prevent and treat Alzheimer's disease.

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