Alzheimer's disease (AD) is the most common form of dementia with global burden 
projected to triple by 2050. It incurs significant biopsychosocial burden 
worldwide with limited treatment options. Aducanumab is the first monoclonal 
antibody recently approved by the US-FDA for mild AD through the accelerated 
approval pathway. It is the first molecule to be approved for AD since 2003 and 
carries with it a therapeutic promise for the future. As the definition of AD 
has evolved from a pathological entity to a Clinico-biological construct over 
the years, the amyloid-β (Aβ) pathway has been increasingly implicated in its 
pathogenesis. The approval of Aducanumab is based on reduction of the Aβ load in 
the brain, which forms a surrogate marker for this pathway. The research 
populace has, however, been globally divided by skepticism and hope regarding 
this approval. Failure to meet clinical endpoints in the trials, alleged 
transparency issues, cost-effectiveness, potential adverse effects, need for 
regular monitoring, and critique of 'amyloid cascade hypothesis' itself are the 
main caveats concerning the antibody. With this controversy in background, this 
paper critically looks at antibody research in AD therapeutics, evidence, and 
evolution of Aducanumab as a drug and the potential clinical implications of its 
use in future. While the efficacy of this monoclonal antibody in AD stands as a 
test of time, based on the growing evidence it is vital to rethink and explore 
alternate pathways of pathogenesis (oxidative stress, neuroinflammation, 
cholesterol metabolism, vascular factors, etc.) as possible therapeutic targets 
that may help elucidate the enigma of this complex yet progressive and 
debilitating neurodegenerative disorder.