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![]() Vol.2, No.2, 49-50 (2013) Advances in Alzheimer ’s Disease http://dx.doi.org/10.4236/aad.2013.22006 Editorial Advances in Alzheimer’s disease (AAD): Standing firm at its first anniversary Xiao-Xin Yan Department of Anatomy and Neurobiology, Central South University Xiangya School of Medicine, Changsha, China; Corresponding Author: [email protected] Received 22 April 2013; revised 24 May 2013; accepted 2 June 2013 Copyright © 2013 Xiao-Xin Yan. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Advances in Alzheimer’s Disease (AAD) is an inter- national journal launched last year, dedicated to promote basic, translational and clinical research on Alzheimer’s Disease (AD) and brain aging (http://www.scirp.org/journal/aad/). On its first anniver- sary, the journal has made substantial achievements and shows a great promise for its future. AAD published the first issue on June 26 last year, followed by the second and third issues in September and December. The first issue of this year was published in March as scheduled. The current issue publishes 3 origin al and review articles. The published papers were contributed by investigators over the world, mostly outside China, covering broad and diverse topics on AD, from mechanistic study to disease diagnosis, care and treatment. These papers have attracted considerable attention in the field, with total views near 40 thousand and full article downloads over 6 thousand to date. AD is the most common type of dementia in the eld- erly. It attacks individuals aged over 65 in most cases, at a prevalence around 5%, which doubles every decade as the age goes further up. In 2013, an estimated 5 million Americans aged 65 and older have AD. The advances in modern medicine and the improvement in social and envi ronmental conditions will further increase human life- expectancy in the coming years, so do for the number of people who will develop this neurodegenerative disease. It is projected that 14 million Americans will live with AD by 2050 (http://www.alz.org/alzheimers_disease_facts_and_figur es.asp?type=alzchptfooter) [1,2]. The situation in China is perhaps even worse and more alarming because of its population in the world, which is rapidly aging. While there is little official epidemiological record, China may already have more than 6 - 8 million AD patients today. What’s more, the overall life-expectancy for Chinese is now about 7 6 y ears (http://en.wikipedia.org/wiki/List_of_ countries_by_life_ expectancy), but it will catch up the current mid-80s re- cords in most western/developed countries within 10 years or so. Together with other problems and d ifficulties (e.g., the one-child policy), China may soon face one of the greatest socioeconomic and healthcare challenges in her journey to modernization (http://charls.ccer.edu.cn). AD is pathologically characterized by amyloid plaques, neurofibrillary tangles, neuritic pathology, gliosis, and neuronal and synaptic loss in vulnerable brain regions especially in the limbic and neocortical areas [3-5]. Ag- ing is the greatest risk factor, while vascular and meta- bolic deficits, trauma, inflammation, environmental in- sults, genetic predisposition, and physiological “wasting” of cognitive and physical reserve are also potential etio- logical factors. Many theories have been proposed for the pathogenesis of this disease. Among all, the amyloid hypothesis emphasizes accumulation of β-amyloid pep- tides (Aβ) being the leading pathogenic factor. The mi- tochondria/metabolic stress cascade hypothesis considers age-inherent metabolic failure or oxidative damages to mitochondrial DNA, RNA, lipid and protein as the pri- mary pathogenic mechanism. The cognitive reserve hy- pothesis suggests that reduced brain use plays an impor- tant role in dementia and AD development. The calcium hypothesis posits Ca2+ homeostatic deregulation contrib- uting to neuronal death and functional decline in brain aging and AD [5-9]. Evidence exists in supporting each of these hypotheses, reflecting the nature of complexity and multi-dimensional abnormalities of this disease. At present, efforts are particularly needed to identify the fundamental molecular/cellular mechanism that may unify the risk factors, pathological manifestations and functional loss in this disease [8 ,9]. Because th ere are no Copyright © 2013 SciRes. OPEN A CCESS ![]() X.-X. Yan / Advances in Alzheimer’s Disease 2 (2013) 49-50 50 available treatments, joint efforts at governmental, aca- demic, clinical and industrial levels are urgently needed to fight against AD across the globe [10]. AAD is one of the journals spo nsored by the Scien tific Research Publishing group headquartered in Wuhan, China. It is the first, and in fact, currently the only spe- cialty journal in the AD field in China. It was launched under the philosophy of free share and use of scientific information. This open-access online journal has a wor- ld-wide representative panel of editorial board members, who, together with external review er s, carry ou t v igoro us and fair evaluation on each submitted manuscript. AAD charges a very affordable publication fee for accepted papers, and manuscripts in all aspects of AD are consid- ered for publication. This journ al is currently indexed by a number of world-class databases/searching engines including CrossRef and Google Scholar (http://www.scirp.org/journal/aad/). Besides its internet accessibility, AAD is now broadly distributed via the library system among universities in mainland China as well as many institutions over the wo rld. The editorial team and publisher are greatly encour- aged by the achievements through the first year of opera- tion, and we expect a healthy growth of this journal in the future. As a part of global effort in combating neu- rodegenerative diseases and improving human life in the world, AAD seeks to serve a unique and important in- ternational platform for scientific communication in AD research, prevention and therapy. REFERENCES [1] Hampel, H., Prvulovic, D., Teipel, S., Jessen, F., Luck- haus, C., Frolich, L., Riepe, M.W., Dodel, R., Leyhe, T., Bertram, L., Hoffmann, W. and Faltraco, F. (2011) The future of Alzheimer’s disease: The next 10 years. Pro- gress in Neurobiology, 95, 718-728. doi:10.1016/j.pneurobio.2011.11.008 [2] Contino, M., Cantore, M., Leopoldo, M. and Colabufo, N.A. (2013) Biomarkers for the early diagnosis of Alz- heimer’s disease: The challenge of XXI century. Ad- vances in Alzheimer’s Disease, 1, 13-30. doi:10.4236/aad.2013.21003 [3] Braak, H. and Del Tredici, K. (2012) Where, when, and in what form does sporadic Alzheimer’s disease begin? Current Opinion in Neurology, 25, 708-714. doi:10.1097/WCO.0b013e32835a3432 [4] Cai, Y., Xiong, K., Zhang, X.M., Ca i, H., Lu o, X.G., Feng, J.C., Clough, R.W., Struble, R.G., Patrylo, P.R., Chu, Y., Kordower, J.H. and Yan, X.X. (2010) β-Secretase-1 ele- vation in aged monkey and Alzheimer’s disease human cerebral cortex occurs around the vasculature in partner- ship with multisystem axon terminal pathogenesis and β-amyloid accumulation. European Journal of Neurosci- ence, 32, 1223-1238. doi: 10 .1111 /j .1 460 -9568.2010.07376.x [5] Radak, Z., Hart, N., Sarga, L., Koltai, E., Atalay, M., Ohno, H. and Boldogh, I. (2010) Exercise plays a preven- tive role against Alzheimer’s disease. Journal of Alz- heimers Disease, 20, 777-783. [6] Stern, Y. (2012) Cognitive reserve in ageing and Alz- heimer ’s disease. Lancet Neurology, 11, 1006-1012. doi:10.1016/S1474-4422(12)70191-6 [7] Skaper, S.D. (2012) Alzheimer’s disease and amyloid: Culprit or coincidence? International Review of Neurobi- ology, 102, 277-316. doi:10.1016/B978-0-12-386986-9.00011-9 [8] Swerdlow, R.H. (2012) Alzheimer’s disease pathologic cascades: Who comes first, what drives what. Neurotoxic- ity Research, 22, 182-194. doi:10.1007/s12640-011-9272-9 [9] Marques, S.C., Oliveira. C.R., Outeiro. T.F. and Pereira. C.M. (2010) Alzheimer’s disease: The quest to under- stand complexity. Journal of Alzheimers Disease, 21, 373-383. [10] Mullane, K. and Williams, M. (2013) Alzheimer’s thera- peutics: Continued clinical failures question the validity of the amyloid hypothesis—But what lies beyond? Bio- chemical Pharmacology, 85, 289-305. doi:10.1016/j.bcp.2012.11.014 Copyright © 2013 SciRes. OPEN A CCESS |



