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2016, Vol.7  No.4

ISSN 2152-5250
Since 2010
2017 impact factor: 5.058
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  • Table of Content
      01 August 2016, Volume 7 Issue 4 Previous Issue    Next Issue
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    Original Article
    Brain Atrophy, Anti-Smooth Muscle Antibody and Cognitive Impairment: An Association Study
    Giulia Paroni, Michele Lauriola, Andrea Fontana, Grazia D’Onofrio, Filomena Ciccone, Francesco Paris, Leandro Cascavilla, Maria Urbano, Carolina Gravina, Massimiliano Copetti, Antonio Greco
    Aging and disease. 2016, 7 (4): 318-325.   DOI: 10.14336/AD.2015.1124
    Abstract   HTML   PDF (656KB) ( 1213 )

    Cortical atrophy, neuronal loss, beta-amyloid deposition, neuritic plaques, and neurofibrillary tangles are neuropathological key features in the Alzheimer’s disease (AD). Antibodies against beta-amyloid, neurotransmitters, microvascular endothelium components and microglial cells have been detected in AD serum suggesting that AD could be another autoimmune disease and provides a link between vascular pathology, endothelium dysfunction and neuronal cells death. Aim of the present study was to evaluate the association between autoantibody profile and cognitive impairment in geriatric patients, accounting for ApoE genotype as a potential confounding factor. Three hundred and forty-four geriatric patients, attending the clinic for the cognitive decline, underwent a biochemical and immunological profile, chest X-ray, cerebral computed tomography scan and complete cognitive evaluation. All patients were also screened for the ApoE genotype. A significantly higher prevalence of Anti-Smooth Muscle Antibody (ASMA) positivity was found in 89/204 (43.63%) patients with diagnosed neuroradiological signs of cerebral atrophy compared with 15/140 (10.71%) patients without the condition (p<0.001). Multivariable logistic model evidenced that such association was independent of patient’s age, gender and Mini-Mental State Examination (OR=8.25, 95%CI: 4.26-15.99) and achieved a good discriminatory power (c-statistic=0.783). Results were also independent of ApoE genotype, which resulted not associated both with the presence of brain atrophy and with the presence of ASMA positivity. Our results shows a strong association between brain atrophy and ASMA positivity and are consistent with several studies that focused attention on the mechanisms of endothelial immune response in the development of dementia.

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    Ischemia-induced Angiogenesis is Attenuated in Aged Rats
    Tang Yaohui, Wang Liuqing, Wang Jixian, Lin Xiaojie, Wang Yongting, Jin Kunlin, Yang Guo-Yuan
    Aging and disease. 2016, 7 (4): 326-335.   DOI: 10.14336/AD.2015.1125
    Abstract   HTML   PDF (1968KB) ( 1107 )

    To study whether focal angiogenesis is induced in aged rodents after permanent distal middle cerebral artery occlusion (MCAO), young adult (3-month-old) and aged (24-month-old) Fisher 344 rats underwent MCAO and sacrificed up to two months after MCAO. Immunohistochemistry and synchrotron radiation microangiography were performed to examine the number of newly formed blood vessels in both young adult and aged rats post-ischemia. We found that the number of capillaries and small arteries in aged brain was the same as young adult brain. In addition, we found that after MCAO, the number of blood vessels in the peri-infarct region of ipsilateral hemisphere in aged ischemic rats was significantly increased compared to the aged sham rats (p<0.05). We also confirmed that ischemia-induced focal angiogenesis occurred in young adult rat brain while the blood vessel density in young adult ischemic brain was significantly higher than that in the aged ischemic brain (p<0.05). Our data suggests that focal angiogenesis in aged rat brain can be induced in response to ischemic brain injury, and that aging impedes brain repairing and remodeling after ischemic stroke, possible due to the limited response of angiogenesis.

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    Inhibition of Endoplasmic Reticulum Stress is Involved in the Neuroprotective Effect of bFGF in the 6-OHDA-Induced Parkinson’s Disease Model
    Cai Pingtao, Ye Jingjing, Zhu Jingjing, Liu Dan, Chen Daqing, Wei Xiaojie, Johnson Noah R., Wang Zhouguang, Zhang Hongyu, Cao Guodong, Xiao Jian, Ye Junming, Lin Li
    Aging and disease. 2016, 7 (4): 336-449.   DOI: 10.14336/AD.2016.0117
    Abstract   HTML   PDF (1206KB) ( 1197 )

    Parkinson's disease (PD) is a progressive neurodegenerative disorder with complicated pathophysiologic mechanisms. Endoplasmic reticulum (ER) stress appears to play a critical role in the progression of PD. We demonstrated that basic fibroblast growth factor (bFGF), as a neurotropic factor, inhibited ER stress-induced neuronal cell apoptosis and that 6-hydroxydopamine (6-OHDA)-induced ER stress was involved in the progression of PD in rats. bFGF administration improved motor function recovery, increased tyrosine hydroxylase (TH)-positive neuron survival, and upregulated the levels of neurotransmitters in PD rats. The 6-OHDA-induced ER stress response proteins were inhibited by bFGF treatment. Meanwhile, bFGF also increased expression of TH. The administration of bFGF activated the downstream signals PI3K/Akt and Erk1/2 in vivo and in vitro. Inhibition of the PI3K/Akt and Erk1/2 pathways by specific inhibitors partially reduced the protective effect of bFGF. This study provides new insight towards bFGF translational drug development for PD involving the regulation of ER stress.

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    Deletion of Nuclear Factor kappa B p50 Subunit Decreases Inflammatory Response and Mildly Protects Neurons from Transient Forebrain Ischemia-induced Damage
    Rolova Taisia, Dhungana Hiramani, Korhonen Paula, Valonen Piia, Kolosowska Natalia, Konttinen Henna, Kanninen Katja, Tanila Heikki, Malm Tarja, Koistinaho Jari
    Aging and disease. 2016, 7 (4): 450-465.   DOI: 10.14336/AD.2015.1123
    Abstract   HTML   PDF (1627KB) ( 810 )

    Transient forebrain ischemia induces delayed death of the hippocampal pyramidal neurons, particularly in the CA2 and medial CA1 area. Early pharmacological inhibition of inflammatory response can ameliorate neuronal death, but it also inhibits processes leading to tissue regeneration. Therefore, research efforts are now directed to modulation of post-ischemic inflammation, with the aim to promote beneficial effects of inflammation and limit adverse effects. Transcription factor NF-κB plays a key role in the inflammation and cell survival/apoptosis pathways. In the brain, NF-κB is predominantly found in the form of a heterodimer of p65 (RelA) and p50 subunit, where p65 has a transactivation domain while p50 is chiefly involved in DNA binding. In this study, we subjected middle-aged Nfkb1 knockout mice (lacking p50 subunit) and wild-type controls of both sexs to 17 min of transient forebrain ischemia and assessed mouse performance in a panel of behavioral tests after two weeks of post-operative recovery. We found that ischemia failed to induce clear memory and motor deficits, but affected spontaneous locomotion in genotype- and sex-specific way. We also show that both the lack of the NF-κB p50 subunit and female sex independently protected CA2 hippocampal neurons from ischemia-induced cell death. Additionally, the NF-κB p50 subunit deficiency significantly reduced ischemia-induced microgliosis, astrogliosis, and neurogenesis. Lower levels of hippocampal microgliosis significantly correlated with faster spatial learning. We conclude that NF-κB regulates the outcome of transient forebrain ischemia in middle-aged subjects in a sex-specific way, having an impact not only on neuronal death but also specific inflammatory responses and neurogenesis.

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    Review Article
    Mobility-Related Consequences of Reduced Lower-Extremity Peripheral Nerve Function with Age: A Systematic Review
    Ward Rachel E., Caserotti Paolo, Cauley Jane A., Boudreau Robert M., Goodpaster Bret H., Vinik Aaron I., Newman Anne B., Strotmeyer Elsa S.
    Aging and disease. 2016, 7 (4): 466-478.   DOI: 10.14336/AD.2015.1127
    Abstract   HTML   PDF (837KB) ( 1049 )

    The objective of this study is to systematically review the relationship between lower-extremity peripheral nerve function and mobility in older adults. The National Library of Medicine (PubMed) was searched on March 23, 2015 with no limits on publication dates. One reviewer selected original research studies of older adults (≥65 years) that assessed the relationship between lower-extremity peripheral nerve function and mobility-related outcomes. Participants, study design and methods of assessing peripheral nerve impairment were evaluated and results were reported and synthesized. Eight articles were identified, including 6 cross-sectional and 2 longitudinal studies. These articles investigated 6 elderly cohorts (4 from the U.S. and 2 from Italy): 3 community-dwelling (including 1 with only disabled women and 1 without mobility limitations at baseline), 1 with both community-dwelling and institutionalized residents, 1 from a range of residential locations, and 1 of patients with peripheral arterial disease. Mean ages ranged from 71-82 years. Nerve function was assessed by vibration threshold (n=2); sensory measures and clinical signs and symptoms of neuropathy (n=2); motor nerve conduction (n=1); and a combination of both sensory measures and motor nerve conduction (n=3). Each study found that worse peripheral nerve function was related to poor mobility, although relationships varied based on the nerve function measure and mobility domain assessed. Six studies found that the association between nerve function and mobility persisted despite adjustment for diabetes. Evidence suggests that peripheral nerve function impairment at various levels of severity is related to poor mobility independent of diabetes. Relationships varied depending on peripheral nerve measure, which may be particularly important when investigating specific biological mechanisms. Future research needs to identify risk factors for peripheral nerve decline beyond diabetes, especially those common in late-life and modifiable. Interventions to preserve nerve function should be investigated with regard to their effect on postponing or preventing disability in older adults.

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    Pathophysiological Function of ADAMTS Enzymes on Molecular Mechanism of Alzheimer’s Disease
    Gurses Murat Serdar, Ural Mustafa Numan, Gulec Mehmet Akif, Akyol Omer, Akyol Sumeyya
    Aging and disease. 2016, 7 (4): 479-490.   DOI: 10.14336/AD.2016.0111
    Abstract   HTML   PDF (963KB) ( 829 )

    The extracellular matrix (ECM) is an environment that has various enzymes attended in regeneration and restoration processes which is very important to sustain physiological and biological functions of central nervous system (CNS). One of the participating enzyme systems in ECM turnover is matrix metalloproteinases. A disintegrin-like and metalloproteinase with thrombospondin type 1 motifs (ADAMTS) is a unique family of ECM proteases found in mammals. Components of this family may be distinguished from the ADAM (A Disintegrin and Metalloproteinase) family based on the multiple copies of thrombospondin 1-like repeats. The considerable role of the ADAMTS in the CNS continues to develop. Evidences indicate that ADAMTS play an important role in neuroplasticity as well as nervous system pathologies such as Alzheimer’s disease (AD). It is hopeful and possible that ADAMTS family members may be utilized to develop therapies for CNS pathologies, ischemic injuries, neurodegenerative and neurological diseases. To understand and provide definitive data on ADAMTS to improve structural and functional recovery in CNS injury and diseases, this review aimed to enlighten the subject extensively to reach certain information on metalloproteinases and related molecules/enzymes. It will be interesting to examine how ADAMTS expression and action would affect the initiation/progression of above-mentioned clinical situations, especially AD.

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    Novel Insights into Acid-Sensing Ion Channels: Implications for Degenerative Diseases
    Zhou Ren-Peng, Wu Xiao-Shan, Wang Zhi-Sen, Xie Ya-Ya, Ge Jin-Fang, Chen Fei-Hu
    Aging and disease. 2016, 7 (4): 491-501.   DOI: 10.14336/AD.2015.1213
    Abstract   HTML   PDF (1236KB) ( 1125 )

    Degenerative diseases often strike older adults and are characterized by progressive deterioration of cells, eventually leading to tissue and organ degeneration for which limited effective treatment options are currently available. Acid-sensing ion channels (ASICs), a family of extracellular H+-activated ligand-gated ion channels, play critical roles in physiological and pathological conditions. Aberrant activation of ASICs is reported to regulate cell apoptosis, differentiation and autophagy. Accumulating evidence has highlighted a dramatic increase and activation of ASICs in degenerative disorders, including multiple sclerosis, Parkinson’s disease, Huntington’s disease, intervertebral disc degeneration and arthritis. In this review, we have comprehensively discussed the critical roles of ASICs and their potential utility as therapeutic targets in degenerative diseases.

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    Danggui-Shaoyao-San: New Hope for Alzheimer's Disease
    Fu Xin, Wang QiuHong, Wang ZhiBin, Kuang HaiXue, Jiang Pinghui
    Aging and disease. 2016, 7 (4): 502-513.   DOI: 10.14336/AD.2015.1220
    Abstract   HTML   PDF (985KB) ( 1516 )

    Danggui-Shaoyao-San (DSS), also called Toki-shakuyaku-san (TJ-23) or Dangguijakyak-san (DJS), is a well-known herbal formula (Angelica sinensis (Oliv.) Diels., Ligusticum chuanxiong Hort., Paeonia lactiflora pall., Poria cocos (Schw.) Wolf, Alisma orientalis (Sam.) Juzep., Atractylodes macrocephala Koidz.), which has been widely used in oriental countries for the treatment of various gynecological diseases. Recent studies show that DSS has an effect on free radical-mediated neurological diseases and exhibits anti-inflammatory and antioxidant activities and reduces cell apoptosis in the hippocampus. In addition, DSS mediates the modulation of central monoamine neurotransmitter systems and ameliorates dysfunction of the central cholinergic nervous system and scopolamine-induced decrease in ACh levels. DSS improves the function of the dopaminergic, adrenergic, and serotonergic nervous systems. Interestingly, DSS can alleviate cognitive dysfunction of Alzheimer's disease (AD) patients, suggesting that it is a useful therapeutic agent for AD. This paper reviews the mechanism of DSS for the treatment of AD.

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    The Role of Bone Marrow Microenvironment in Governing the Balance between Osteoblastogenesis and Adipogenesis
    Li Jiao, Liu Xingyu, zuo Bin, Zhang Li
    Aging and disease. 2016, 7 (4): 514-525.   DOI: 10.14336/AD.2015.1206
    Abstract   HTML   PDF (861KB) ( 1069 )

    In the adult bone marrow, osteoblasts and adipocytes share a common precursor called mesenchymal stem cells (MSCs). The plasticity between the two lineages has been confirmed over the past decades, and has important implications in the etiology of bone diseases such as osteoporosis, which involves an imbalance between osteoblasts and adipocytes. The commitment and differentiation of bone marrow (BM) MSCs is tightly controlled by the local environment that maintains a balance between osteoblast lineage and adipocyte. However, pathological conditions linked to osteoporosis can change the BM microenvironment and shift the MSC fate to favor adipocytes over osteoblasts, and consequently decrease bone mass with marrow fat accumulation. This review discusses the changes that occur in the BM microenvironment under pathological conditions, and how these changes affect MSC fate. We suggest that manipulating local environments could have therapeutic implications to avoid bone loss in diseases like osteoporosis.

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    Population Aging in the European Information Societies: Towards a Comprehensive Research Agenda in eHealth Innovations for Elderly
    Vancea Mihaela, Solé-Casals Jordi
    Aging and disease. 2016, 7 (4): 526-539.   DOI: 10.14336/AD.2015.1214
    Abstract   HTML   PDF (776KB) ( 1224 )

    Population ageing is one of the major social and economic challenges of our contemporary societies. With the advent of the information society, new research and technological developments have been promoted in the field of assistive technologies and information and communication technologies of benefit to elderly people. This article examines the potentialities of new informatics developments in generating solutions to better address elderly people’s daily-life, especially those with chronic illness and/or low autonomy. The authours attempt to propose a research agenda, by exposing various strengts and weaknesses of eHealth innovations for elderly, mainly grounded in secondary sources analysis.

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  Editors-in-Chief  
Kunlin Jin, M.D., Ph.D., Professor
Ashok K. Shetty, Ph.D., Professor
David A. Greenberg, M.D., Ph.D., Professor
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