Vol.2, No.2, 49-50 (2013) Advances in Alzheimer ’s Disease
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: yanxiaoxin@csu.edu.cn
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
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
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
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.
[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.
[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 Alzheimers Disease, 1, 13-30.
[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.
[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-
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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.
[7] Skaper, S.D. (2012) Alzheimer’s disease and amyloid:
Culprit or coincidence? International Review of Neurobi-
ology, 102, 277-316.
[8] Swerdlow, R.H. (2012) Alzheimer’s disease pathologic
cascades: Who comes first, what drives what. Neurotoxic-
ity Research, 22, 182-194.
[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,
[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-
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Copyright © 2013 SciRes. OPEN A CCESS