Editorial Advances in Alzheimer’s Disease: From Bench to Bedside

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. In 1906, Alois Alzheimer first documented the case of Auguste Deter, a patient with a combination of cogni-tive deficits, psychiatric symptoms, and microscopic brain lesions. This histopathological and clinical constellation was then designated by Emil Kraepelin as Alzheimer’s disease (AD) [1]. Nowadays, AD became the most common pro-gressive neurodegenerative disease and the most common form of dementia among the elderly [2, 3]. In the clinic, the late-onset AD (LOAD) accounts for 95 % of all AD cases and is currently considered as a genetic complex disorder that is probably caused by a combination of multiple risk alleles and environmental factors [4]. To date, APOE is the only unequivocally established susceptibility gene for LOAD [5]. However, it has been estimated that the variations of APOE account for less than 50 % of LOAD risk, suggesting that there are additional genetic risk factors which remain to be uncovered. Recent advances in genetic approaches led to the identification of numerous risk genes for AD, which has greatly extended our knowledge on the genetic components of this disease [6]. In this special issue, the paper entitled “Clinical Genetics of Alzheimer’s Disease ” by Z. Zou et al. outlined these novel susceptibility genes, such as CLU, CR1