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Summary: For more than a century, clinicians have been aware of the devastating neurological condition called Alzheimer’s disease (AD). AD is characterized by the presence of abnormal amyloid protein plaques and tau tangles in the brain. The dominant hypothesis, termed the amyloid hypothesis, attributes AD development to excessive cleavage and accumulation of amyloid precursor protein (APP), leading to brain tissue atrophy. The amyloid hypothesis has greatly influenced AD research and therapeutic endeavors. However, despite significant attention, a complete understanding of amyloid and APP’s roles in disease pathology, progression, and cognitive impairment remains elusive. Recent controversies and several unsuccessful drug trials have called into question whether amyloid is the only neuropathological factor for treatment. To accomplish disease amelioration, we argue that researchers and clinicians may need to take a compounding approach to target amyloid and other factors in the brain, including traditional pharmaceuticals and holistic therapies.