Alzheimer disease is the most common neurodegenerative disease that afflicts mankind. Tremendous efforts have been made in investigating the genetic understanding and molecular pathophysiology of this illness. Disease mainly defined by its pathological attributes including amyloid ? deposits in the form of extracellular amyloid ? (A?) plaques and tau protein aggregates in the form of intracellular neurofibrillary tangles. A central mechanism underlying the formation of both amyloid plaques and neurofibrillary tangles in Alzheimer disease is pathogenic cerebral tau protein aggregation. Though both amyloid plaques and aggregated tau have an essential role in Alzheimer disease pathology and are part of the neuropathological definition of the disease, numerous studies suggest that in these precipitated forms they are relatively biologically inert. Hence, the accumulation of aggregated Aâ in plaques correlates poorly with the clinical status of patients. This review highlights recent advances in molecular and clinical aspects. Metabolic and functional studies by scanning tomography indicate that prominent atrophy and metabolic abnormalities emerged in the posterior cortical regions and medial temporal regions at early stages of Alzheimer disease progression. Several genes including APP, PSEN1, PSEN2 and APOE e4 have been identified to be associated with Alzheimer disease. Some of the latest high thought put technological platforms including genomewide association studies, transcriptomics, proteomics, metabolomics and epigenetics. These approaches are introduced briefly. Many newly identified Alzheimer disease risk genes such as triggering receptor expressed on myeloid cells2 (TREM2) are exclusively expressed, or highly enriched in glial cells. Alzheimer disease pathogenesis involves pathogenic contributions from multiple components and alterations in behaviour of various cell types presented in a model within the central nervous system. Other than TREM2, a few other genes are discovered which are associated with Alzheimer disease but their functions are not known. Since no efficacious drugs are available at present, a systematic approach towards the diverse findings from various platforms will most likely give us understanding of about the disease pattern.