Alzheimer's disease (AD) was first described over 100 years ago and is the most common cause of dementia, affecting 30 million people globally, with prevalence expected to quadruple in 40 years. Currently, there is no effective treatment to delay or slow AD progression. However, recent advances in genetics, biochemistry, and neuroscience have changed our understanding of AD, offering hope that early detection and targeted therapies based on pathogenesis could be effective. AD is characterized by protein aggregation of amyloid-β (Aβ) and tau, which play key roles in pathophysiology. Pathological changes begin 10–20 years before clinical symptoms, and recent biomarkers allow early detection of AD pathology in cognitively normal individuals. These biomarkers, such as Aβ deposition and neurodegeneration, are being used in clinical trials to assess AD risk and potential therapies. AD pathology, including amyloid plaques and neurofibrillary tangles, begins years before clinical symptoms and is associated with cognitive decline. The clinical features of AD include progressive memory loss, cognitive deficits, and behavioral changes. The Clinical Dementia Rating (CDR) system is used to assess dementia severity. AD genetics has revealed that mutations in genes such as APP, PSEN1, and PSEN2 are linked to familial AD (FAD), while APOE ε4 is a major risk factor for late-onset AD (LOAD). APOE ε4 is associated with earlier onset and increased risk of AD and cerebral amyloid angiopathy (CAA). Other genetic factors, along with environmental influences such as head injury, education, and lifestyle, contribute to AD risk. Recent genome-wide association studies (GWAS) have identified new genetic risk factors, including CLU, PICALM, CR1, BIN1, and CD33, which may influence AD pathogenesis through mechanisms involving inflammation, endocytosis, and lipid biology. While APOE is the strongest genetic risk factor, other genes may also play a role in AD. Environmental factors such as physical activity and head injury also influence AD risk. The interaction between genetic and environmental factors is complex, and understanding these interactions is crucial for developing effective therapies. Current research focuses on identifying new therapeutic targets, including γ-secretase modulators (GSMs) and BACE inhibitors, which aim to reduce Aβ production. The challenge remains to translate these findings into effective treatments for AD.Alzheimer's disease (AD) was first described over 100 years ago and is the most common cause of dementia, affecting 30 million people globally, with prevalence expected to quadruple in 40 years. Currently, there is no effective treatment to delay or slow AD progression. However, recent advances in genetics, biochemistry, and neuroscience have changed our understanding of AD, offering hope that early detection and targeted therapies based on pathogenesis could be effective. AD is characterized by protein aggregation of amyloid-β (Aβ) and tau, which play key roles in pathophysiology. Pathological changes begin 10–20 years before clinical symptoms, and recent biomarkers allow early detection of AD pathology in cognitively normal individuals. These biomarkers, such as Aβ deposition and neurodegeneration, are being used in clinical trials to assess AD risk and potential therapies. AD pathology, including amyloid plaques and neurofibrillary tangles, begins years before clinical symptoms and is associated with cognitive decline. The clinical features of AD include progressive memory loss, cognitive deficits, and behavioral changes. The Clinical Dementia Rating (CDR) system is used to assess dementia severity. AD genetics has revealed that mutations in genes such as APP, PSEN1, and PSEN2 are linked to familial AD (FAD), while APOE ε4 is a major risk factor for late-onset AD (LOAD). APOE ε4 is associated with earlier onset and increased risk of AD and cerebral amyloid angiopathy (CAA). Other genetic factors, along with environmental influences such as head injury, education, and lifestyle, contribute to AD risk. Recent genome-wide association studies (GWAS) have identified new genetic risk factors, including CLU, PICALM, CR1, BIN1, and CD33, which may influence AD pathogenesis through mechanisms involving inflammation, endocytosis, and lipid biology. While APOE is the strongest genetic risk factor, other genes may also play a role in AD. Environmental factors such as physical activity and head injury also influence AD risk. The interaction between genetic and environmental factors is complex, and understanding these interactions is crucial for developing effective therapies. Current research focuses on identifying new therapeutic targets, including γ-secretase modulators (GSMs) and BACE inhibitors, which aim to reduce Aβ production. The challenge remains to translate these findings into effective treatments for AD.