Title:Aducanumab in Alzheimer’s Disease: A Critical Update
Volume: 31
Issue: 31
Author(s): Sumel Ashique, Ekta Sirohi, Shubneesh Kumar, Mohd Rihan, Neeraj Mishra, Shvetank Bhatt, Rupesh K. Gautam, Sachin Kumar Singh, Gaurav Gupta*, Dinesh Kumar Chellappan and Kamal Dua*
Affiliation:
- School of Pharmacy, Suresh Gyan Vihar
University, Mahal Road, Jagatpura, Jaipur, India
- Department of Pharmacology, Saveetha Dental College, Saveetha Institute of
Medical and Technical Sciences, Saveetha University, Chennai, India
- Uttaranchal Institute of Pharmaceutical Sciences, Uttaranchal
University, Dehradun, India
- Faculty of Health, Australian Research Centre in Complementary
and Integrative Medicine, University of Technology Sydney, Ultimo 2007, Australia
- Discipline of Pharmacy, Graduate School of Health, University of Technology
Sydney, Sydney, NSW, 2007, Australia
Keywords:
Aducanumab, amyloid plaque, Alzheimer's disease, anti-N-methyl D-aspartate, anti-cholinesterase, inflammation.
Abstract: Alzheimer's disease (AD) is a complex neurological disorder that results in cognitive
decline. The incidence rates of AD have been increasing, particularly among individuals
60 years of age or older. In June 2021, the US FDA approved aducanumab, the first humanized
monoclonal antibody, as a potential therapeutic option for AD. Clinical trials have shown
this drug to effectively target the accumulation of Aβ (beta-amyloid) plaques in the brain, and
its effectiveness is dependent on the dosage and duration of treatment. Additionally, aducanumab
has been associated with improvements in cognitive function. Biogen, the pharmaceutical
company responsible for developing and marketing aducanumab, has positioned it as
a potential breakthrough for treating cerebral damage in AD. However, the drug has raised
concerns due to its high cost, limitations, and potential side effects. AD is a progressive neurological
condition that affects memory, cognitive function, and behaviour. It significantly impacts
the quality of life of patients and caregivers and strains healthcare systems. Ongoing research
focuses on developing disease-modifying therapies that can halt or slow down AD progression.
The pathogenesis of AD involves various molecular cascades and signaling pathways.
However, the formation of extracellular amyloid plaques is considered a critical mechanism
driving the development and progression of the disease. Aducanumab, as a monoclonal
antibody, has shown promising results in inhibiting amyloid plaque formation, which is the
primary pathological feature of AD. This review explores the signaling pathways and molecular
mechanisms through which aducanumab effectively prevents disease pathogenesis in AD.
