Alzheimer's disease (AD) is the most common cause of dementia, affecting an estimated 30 million people worldwide, with a projected quadrupling by 2050. Despite major scientific advances in genetics, biochemistry, cell biology, and neuroscience over the past 25 years, there is still no effective treatment to delay the onset or slow the progression of AD. The review highlights the clinical and pathological features of AD, emphasizing its global public health impact. It discusses the challenges in translating scientific findings into new treatments, focusing on the role of amyloid-β (Aβ) and tau proteins in AD pathogenesis. Recent advances in biomarker detection have enabled the early detection of AD pathology in cognitively normal individuals, but the field faces the challenge of identifying high-risk populations for clinical trials. The review also explores the genetic and environmental factors contributing to AD, including the identification of risk genes such as *APP*, *PSEN1*, *PSEN2*, and *APOE*. The connection between Aβ and tau proteins is discussed, along with the potential for therapeutic interventions targeting these proteins. The review concludes by emphasizing the need for further research to understand the complex interactions between genetic and environmental factors in AD pathogenesis.Alzheimer's disease (AD) is the most common cause of dementia, affecting an estimated 30 million people worldwide, with a projected quadrupling by 2050. Despite major scientific advances in genetics, biochemistry, cell biology, and neuroscience over the past 25 years, there is still no effective treatment to delay the onset or slow the progression of AD. The review highlights the clinical and pathological features of AD, emphasizing its global public health impact. It discusses the challenges in translating scientific findings into new treatments, focusing on the role of amyloid-β (Aβ) and tau proteins in AD pathogenesis. Recent advances in biomarker detection have enabled the early detection of AD pathology in cognitively normal individuals, but the field faces the challenge of identifying high-risk populations for clinical trials. The review also explores the genetic and environmental factors contributing to AD, including the identification of risk genes such as *APP*, *PSEN1*, *PSEN2*, and *APOE*. The connection between Aβ and tau proteins is discussed, along with the potential for therapeutic interventions targeting these proteins. The review concludes by emphasizing the need for further research to understand the complex interactions between genetic and environmental factors in AD pathogenesis.