Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and cognitive decline, with hallmark pathological features including senile plaques and neurofibrillary tangles (NFTs). Initially described by Alois Alzheimer in 1907, AD was later distinguished from other dementias, such as vascular dementia and Lewy body dementia. While AD was historically classified based on age of onset, it is now recognized as a single entity with increasing prevalence after age 65. Diagnosis requires clinical evidence of memory impairment and dysfunction in at least one other cognitive domain, along with social or occupational dysfunction. However, no reliable peripheral biomarker exists, and a definitive diagnosis requires postmortem examination, often using PET scans with Pittsburgh Compound B (PiB) to detect amyloid-β (Aβ) plaques. Despite advancements, PiB has limitations in differentiating symptomatic AD from asymptomatic controls with amyloid plaques. The concept of mild cognitive impairment (MCI) has been introduced to identify early-stage AD, but MCI is not a distinct entity and lacks a clear pathological basis. AD is relentlessly progressive, leading to severe cognitive and functional decline, with the most common cause of death being pneumonia. The disease affects approximately 70% of all dementia cases, with incidence increasing with age. The global prevalence is projected to rise significantly, driven by aging populations. Risk factors include age, family history, genetic factors (e.g., APOE ε4), and vascular disease. Pathologically, AD is characterized by senile plaques and NFTs, with NFTs being more closely associated with clinical disease. The distinction between AD and aging pathology is complex, with some cases of cognitive intact individuals showing AD pathology. The Braak staging system highlights the progression of NFTs from the transentorhinal region to the isocortex, while the NIA-Reagan criteria classify cases based on the likelihood of AD. Cerebral amyloid angiopathy (CAA) is a common feature in AD, contributing to vascular complications. Despite the amyloid cascade hypothesis, the relationship between CAA and AD remains debated, with evidence suggesting that CAA may not be a primary cause of cognitive decline in all cases. The role of synapse loss in AD is increasingly recognized, though its significance in diagnosis remains limited. The pathogenesis of AD involves complex interactions between amyloid-β, tau, and vascular factors, with ongoing research aiming to clarify these mechanisms and develop effective treatments.Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and cognitive decline, with hallmark pathological features including senile plaques and neurofibrillary tangles (NFTs). Initially described by Alois Alzheimer in 1907, AD was later distinguished from other dementias, such as vascular dementia and Lewy body dementia. While AD was historically classified based on age of onset, it is now recognized as a single entity with increasing prevalence after age 65. Diagnosis requires clinical evidence of memory impairment and dysfunction in at least one other cognitive domain, along with social or occupational dysfunction. However, no reliable peripheral biomarker exists, and a definitive diagnosis requires postmortem examination, often using PET scans with Pittsburgh Compound B (PiB) to detect amyloid-β (Aβ) plaques. Despite advancements, PiB has limitations in differentiating symptomatic AD from asymptomatic controls with amyloid plaques. The concept of mild cognitive impairment (MCI) has been introduced to identify early-stage AD, but MCI is not a distinct entity and lacks a clear pathological basis. AD is relentlessly progressive, leading to severe cognitive and functional decline, with the most common cause of death being pneumonia. The disease affects approximately 70% of all dementia cases, with incidence increasing with age. The global prevalence is projected to rise significantly, driven by aging populations. Risk factors include age, family history, genetic factors (e.g., APOE ε4), and vascular disease. Pathologically, AD is characterized by senile plaques and NFTs, with NFTs being more closely associated with clinical disease. The distinction between AD and aging pathology is complex, with some cases of cognitive intact individuals showing AD pathology. The Braak staging system highlights the progression of NFTs from the transentorhinal region to the isocortex, while the NIA-Reagan criteria classify cases based on the likelihood of AD. Cerebral amyloid angiopathy (CAA) is a common feature in AD, contributing to vascular complications. Despite the amyloid cascade hypothesis, the relationship between CAA and AD remains debated, with evidence suggesting that CAA may not be a primary cause of cognitive decline in all cases. The role of synapse loss in AD is increasingly recognized, though its significance in diagnosis remains limited. The pathogenesis of AD involves complex interactions between amyloid-β, tau, and vascular factors, with ongoing research aiming to clarify these mechanisms and develop effective treatments.