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The Effect of Aquaporin-4 Knockout on Interstitial Fluid Flow and the Structure of the Extracellular Space in the Deep Brain
It has been reported that aquaporin-4 (AQP4) deficiency impairs transportation between the cerebrospinal fluid and interstitial fluid (ISF) as well as the clearance of interstitial solutes in the superficial brain. Howev. . .
DOI: 10.14336/AD.2017.1115  
SDF-1/CXCR7 Chemokine Signaling is Induced in the Peri-Infarct Regions in Patients with Ischemic Stroke
Stromal-derived factor-1 (SDF-1, also known as CXCL12) and its receptors CXCR4 and CXCR7 play important roles in brain repair after ischemic stroke, as SDF-1/ CXCR4/CXCR7 chemokine signaling is critical for recruiting st. . .
DOI: 10.14336/AD.2017.1112  
  • Current Issue
      01 October 2017, Volume 8 Issue 5 Previous Issue   
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    Original Article
    Aging Systemic Milieu Impairs Outcome after Ischemic Stroke in Rats
    Mengxiong Pan,Peng Wang,Chengcai Zheng,Hongxia Zhang,Siyang Lin,Bei Shao,Qichuan Zhuge,Kunlin Jin
    A&D. 2017, 8 (5): 519-530.   DOI: 10.14336/AD.2017.0710
    Abstract   HTML   PDF (1568KB) ( 136 )

    Compelling evidence indicates that factors in the blood can profoundly reverse aging-related impairments, as exposure of aged mice to young blood rejuvenates adult stem cell function, improves cognition, and ameliorates cardiac hypertrophy. Systemic factors from mice can also extend the life span of a partner exposed to a lethal treatment or disease. These findings suggest that the systemic milieu of a healthy young partner may be beneficial for an aged organism. However, it is unknown whether a healthy young systemic milieu can improve functional recovery after ischemic stroke. Intraperitoneal administration of young plasma into aged rats after ischemic stroke induced by distal middle cerebral artery occlusion (dMCAO) reduced infarct volume and motor impairment, compared with vehicle group. On the contrary, intraperitoneal administration of plasma from aged rats into young ischemic rats worsened brain injury and motor deficits. Using a proteomic approach, we found that haptoglobin levels were significantly increased in serum of aged rats and that intraperitoneal administration of haptoglobin impaired outcome after ischemic stroke in young rats. Our data suggest that the aging systemic milieu plays a critical role in functional outcome after ischemic stroke.

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    Promoting Neurovascular Recovery in Aged Mice after Ischemic Stroke - Prophylactic Effect of Omega-3 Polyunsaturated Fatty Acids
    Mengfei Cai,Wenting Zhang,Zhongfang Weng,R. Anne Stetler,Xiaoyan Jiang,Yejie Shi,Yanqin Gao,Jun Chen
    A&D. 2017, 8 (5): 531-545.   DOI: 10.14336/AD.2017.0520
    Abstract   HTML   PDF (1663KB) ( 99 )

    The aged population is among the highest at risk for ischemic stroke, yet most stroke patients of advanced ages (>80 years) are excluded from access to thrombolytic treatment by tissue plasminogen activator, the only FDA approved pharmacological therapy for stroke victims. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) robustly alleviate ischemic brain injury in young adult rodents, but have not yet been studied in aged animals. This study investigated whether chronic dietary supplementation of n-3 PUFAs protects aging brain against cerebral ischemia and improves long-term neurological outcomes. Aged (18-month-old) mice were administered n-3 PUFA-enriched fish oil in daily chow for 3 months before and up to 8 weeks after 45 minutes of transient middle cerebral artery occlusion (tMCAO). Sensorimotor outcomes were assessed by cylinder test and corner test up to 35 days and brain repair dynamics evaluated immunohistologically up to 56 days after tMCAO. Mice receiving dietary supplementation of n-3 PUFAs for 3 months showed significant increases in brain ratio of n-3/n-6 PUFA contents, and markedly reduced long-term sensorimotor deficits and chronic ischemic brain tissue loss after tMCAO. Mechanistically, n-3 PUFAs robustly promoted post-ischemic angiogenesis and neurogenesis, and enhanced white matter integrity after tMCAO. The Pearson linear regression analysis revealed that the enhancement of neurogenesis and white matter integrity both correlated positively with improved sensorimotor activities after tMCAO. This study demonstrates that prophylactic dietary supplementation of n-3 PUFAs effectively improves long-term stroke outcomes in aged mice, perhaps by promoting post-stroke brain repair processes such as angiogenesis, neurogenesis, and white matter restoration.

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    Parity History Determines a Systemic Inflammatory Response to Spread of Ovarian Cancer in Naturally Aged Mice
    Ulises Urzua,Carlos Chacon,Luis Lizama,Sebastián Sarmiento,Pía Villalobos,Belén Kroxato,Katherine Marcelain,María-Julieta Gonzalez
    A&D. 2017, 8 (5): 546-557.   DOI: 10.14336/AD.2017.0110
    Abstract   HTML   PDF (820KB) ( 96 )

    Aging intersects with reproductive senescence in women by promoting a systemic low-grade chronic inflammation that predisposes women to several diseases including ovarian cancer (OC). OC risk at menopause is significantly modified by parity records during prior fertile life. To date, the combined effects of age and parity on the systemic inflammation markers that are particularly relevant to OC initiation and progression at menopause remain largely unknown. Herein, we profiled a panel of circulating cytokines in multiparous versus virgin C57BL/6 female mice at peri-estropausal age and investigated how cytokine levels were modulated by intraperitoneal tumor induction in a syngeneic immunocompetent OC mouse model. Serum FSH, LH and TSH levels increased with age in both groups while prolactin (PRL) was lower in multiparous respect to virgin mice, a finding previously observed in parous women. Serum CCL2, IL-10, IL-5, IL-4, TNF-α, IL1-β and IL-12p70 levels increased with age irrespective of parity status, but were specifically reduced following OC tumor induction only in multiparous mice. Animals developed hemorrhagic ascites and tumor implants in the omental fat band and other intraperitoneal organs by 12 weeks after induction, with multiparous mice showing a significantly extended survival. We conclude that previous parity history counteracts aging-associated systemic inflammation possibly by reducing the immunosuppression that typically allows tumor spread. Results suggest a partial impairment of the M2 shift in tumor-associated macrophages as well as decreased stimulation of regulatory B-cells in aged mice. This long term, tumor-concurrent effect of parity on inflammation markers at menopause would be a contributing factor leading to decreased OC risk.

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    Uncontrolled Hypertension Increases with Age in an Older Community-Dwelling Chinese Population in Shanghai
    Sheng Peng,Ting Shen,Jie Liu,Brian Tomlinson,Huimin Sun,Xiaoli Chen,Paul Chan,YaShu Kuang,Liang Zheng,Hong Wu,Xugang Ding,Dingguang Qian,Yixin Shen,Pingjin Gao,Huimin Fan,Zhongmin Liu,Yuzhen Zhang
    A&D. 2017, 8 (5): 558-569.   DOI: 10.14336/AD.2016.1220
    Abstract   HTML   PDF (819KB) ( 50 )

    We determined the prevalence of hypertension, medication usage and attainment of blood pressure goals in older (≥65 to <80 years and ≥80 years) urban community-dwelling Chinese subjects. Data were obtained in 3950 subjects (mean age 72.0 years, 1745 male) including 609 subjects aged ≥80 years in the Shanghai Elderly Cardiovascular Health Study (SHECHS). Established cardiovascular disease was present in 7.7% of participants. The prevalence of hypertension was 74.8% overall and it was more than 80% in individuals considered to be in moderate and higher cardiovascular disease risk categories. In hypertensive subjects, 67.1% were on treatment and treatment was more frequent in high and very high cardiovascular risk individuals. Attainment of the systolic blood pressure goal <150 mmHg was 62.9% and was greater in the ≥65 to <80 years group than in the ≥80 years group. The most commonly used antihypertensive treatments were calcium channel blockers (54.2%), followed by angiotensin receptor blockers (43.1%). Diuretics were used in 2.6%. Fixed-dose combination antihypertensive tablets were used in some of the ≥65 to <80 years group (12.4%) and more of the ≥80 years group (18.2%) and 70.9% of the ≥65 to <80 years group and 80.2% of the ≥80 years group were on monotherapy. There were high prevalence and high treatment rates of hypertension, but poor attainment of the systolic blood pressure goal of <150 mmHg, especially in the ≥80 years group of community-dwelling Chinese. Considering that more intensive treatment of hypertension in older subjects may be warranted after recent studies, this might be achieved by more frequent use of combinations of effective therapies and diuretics.

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    The Pathogenesis of Ossification of the Posterior Longitudinal Ligament
    Liang Yan,Rui Gao,Yang Liu,Baorong He,Shemin Lv,Dingjun Hao
    A&D. 2017, 8 (5): 570-582.   DOI: 10.14336/AD.2017.0201
    Abstract   HTML   PDF (938KB) ( 135 )

    Ossification of the posterior longitudinal ligament (OPLL) is a multi-factorial disease involving an ectopic bone formation of spinal ligaments. It affects 0.8-3.0% aging Asian and 0.1-1.7% aging European Caucasian. The ossified ligament compresses nerve roots in the spinal cord and causes serious neurological problems such as myelopathy and radiculopathy. Research in understanding pathogenesis of OPLL over the past several decades have revealed many genetic and non-genetic factors contributing to the development and progress of OPLL. The characterizations of aberrant signaling of bone morphogenetic protein (BMP) and mitogen-activated protein kinases (MAPK), and the pathological phenotypes of OPLL-derived mesenchymal stem cells (MSCs) have provided new insights on the molecular mechanisms underlying OPLL. This paper reviews the recent progress in understanding the pathophysiology of OPLL and proposes future research directions on OPLL.

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    Recognizing Degenerative Aging as a Treatable Medical Condition: Methodology and Policy
    Ilia Stambler
    A&D. 2017, 8 (5): 583-589.   DOI: 10.14336/AD.2017.0130
    Abstract   HTML   PDF (789KB) ( 327 )

    It is becoming increasingly clear that in order to accomplish healthy longevity for the population, there is an urgent need for the research and development of effective therapies against degenerative aging processes underlying major aging-related diseases, including heart disease, neurodegenerative diseases, type 2 diabetes, cancer, pulmonary obstructive diseases, as well as aging-related complications and susceptibilities of infectious communicable diseases. Yet, an important incentive for the research and development of such therapies appears to be the development of clinically applicable and scientifically grounded definitions and criteria for the multifactorial degenerative aging process (or “senility” using the existing ICD category), underlying those diseases, as well as for the safety and effectiveness of interventions against it. Such generally agreed definitions and criteria are currently absent. The devising of such criteria is important not only for the sake of their scientific value and their utility for the development of therapeutic solutions for the aging population, but also to comply with and implement major existing national and international programmatic and regulatory requirements. Some methodological suggestions and potential pitfalls for the development of such criteria are examined.

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    Age-related Impairment of Vascular Structure and Functions
    Xianglai Xu,Brian Wang,Changhong Ren,Jiangnan Hu,David A. Greenberg,Tianxiang Chen,Liping Xie,Kunlin Jin
    A&D. 2017, 8 (5): 590-610.   DOI: 10.14336/AD.2017.0430
    Abstract   HTML   PDF (1248KB) ( 61 )

    Among age-related diseases, cardiovascular and cerebrovascular diseases are major causes of death. Vascular dysfunction is a key characteristic of these diseases wherein age is an independent and essential risk factor. The present work will review morphological alterations of aging vessels in-depth, which includes the discussion of age-related microvessel loss and changes to vasculature involving the capillary basement membrane, intima, media, and adventitia as well as the accompanying vascular dysfunctions arising from these alterations.

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    Cancer and Aging - the Inflammatory Connection
    Adar Zinger,William C Cho,Arie Ben-Yehuda
    A&D. 2017, 8 (5): 611-627.   DOI: 10.14336/AD.2016.1230
    Abstract   HTML   PDF (852KB) ( 132 )

    Aging and cancer are highly correlated biological phenomena. Various cellular processes such as DNA damage responses and cellular senescence that serve as tumor suppressing mechanisms throughout life result in degenerative changes and contribute to the aging phenotype. In turn, aging is considered a pro-tumorigenic state, and constitutes the single most important risk factor for cancer development. However, the causative relations between aging and cancer is not straight forward, as these processes carry contradictory hallmarks; While aging is characterized by tissue degeneration and organ loss of function, cancer is a state of sustained cellular proliferation and gain of new functions. Here, we review the molecular and cellular pathways that stand in the base of aging related cancer. Specifically, we deal with the inflammatory perspective that link these two processes, and suggest possible molecular targets that may be exploited to modify their courses.

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    The Biology of Aging and Cancer: A Brief Overview of Shared and Divergent Molecular Hallmarks
    Jan R. Aunan,William C Cho,Kjetil Søreide
    A&D. 2017, 8 (5): 628-642.   DOI: 10.14336/AD.2017.0103
    Abstract   HTML   PDF (1005KB) ( 232 )

    Aging is the inevitable time-dependent decline in physiological organ function and is a major risk factor for cancer development. Due to advances in health care, hygiene control and food availability, life expectancy is increasing and the population in most developed countries is shifting to an increasing proportion of people at a cancer susceptible age. Mechanisms of aging are also found to occur in carcinogenesis, albeit with shared or divergent end-results. It is now clear that aging and cancer development either share or diverge in several disease mechanisms. Such mechanisms include the role of genomic instability, telomere attrition, epigenetic changes, loss of proteostasis, decreased nutrient sensing and altered metabolism, but also cellular senescence and stem cell function. Cancer cells and aged cells are also fundamentally opposite, as cancer cells can be thought of as hyperactive cells with advantageous mutations, rapid cell division and increased energy consumption, while aged cells are hypoactive with accumulated disadvantageous mutations, cell division inability and a decreased ability for energy production and consumption. Nonetheless, aging and cancer are tightly interconnected and many of the same strategies and drugs may be used to target both, while in other cases antagonistic pleiotrophy come into effect and inhibition of one can be the activation of the other. Cancer can be considered an aging disease, though the shared mechanisms underpinning the two processes remain unclear. Better understanding of the shared and divergent pathways of aging and cancer is needed.

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    Skin Cancer Epidemics in the Elderly as An Emerging Issue in Geriatric Oncology
    Simone Garcovich,Giuseppe Colloca,Pietro Sollena,Bellieni Andrea,Lodovico Balducci,William C. Cho,Roberto Bernabei,Ketty Peris
    A&D. 2017, 8 (5): 643-661.   DOI: 10.14336/AD.2017.0503
    Abstract   HTML   PDF (786KB) ( 51 )

    Skin cancer is a worldwide, emerging clinical need in the elderly white population, with a steady increase in incidence rates, morbidity and related medical costs. Skin cancer is a heterogeneous group of cancers comprising cutaneous melanoma and non-melanoma skin cancers (NMSC), which predominantly affect elderly patients, aged older than 65 years. Melanoma has distinct clinical presentations in the elderly patient and represents a challenging question in terms of clinical management. NMSC includes the basal cell carcinoma and cutaneous squamous cell carcinoma and presents a wide disease spectrum in the elderly population, ranging from low-risk to high-risk tumours, advanced and inoperable disease. Treatment decisions for NMSC are preferentially based on tumour characteristics, patient’s chronological age and physician’s preferences and operational settings. Several treatment options are available for NMSC, from surgery to non-invasive/medical therapies, but patient-based factors, such as geriatric comorbidities and patient’s life expectancy, do not frequently modulate treatment goals. In melanoma, age-related variations in clinical management are significant and may frequently lead to under-treatment, limiting access to advanced surgical and medical treatments. Clinical decision-making in the care of elderly skin cancer patient should ideally implement a geriatric assessment, prioritizing patient-based factors and efficiently differentiating fit from frail cancer patients. Current clinical practice guidelines for NMSC and melanoma only partially address geriatric aspects of cancer care, such as frailty, limited life-expectancy, geriatric comorbidities and treatment compliance. We review the recent evidence on the scope and problem of skin cancer in the elderly population as well as age-related variations in its clinical management, highlighting the potential role of a geriatric approach in optimizing dermato-oncological care.

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    Aging, Metabolism, and Cancer Development: from Peto’s Paradox to the Warburg Effect
    Tia R. Tidwell,Kjetil Søreide,Hanne R. Hagland
    A&D. 2017, 8 (5): 662-676.   DOI: 10.14336/AD.2017.0713
    Abstract   HTML   PDF (1084KB) ( 65 )

    Medical advances made over the last century have increased our lifespan, but age-related diseases are a fundamental health burden worldwide. Aging is therefore a major risk factor for cardiovascular disease, cancer, diabetes, obesity, and neurodegenerative diseases, all increasing in prevalence. However, huge inter-individual variations in aging and disease risk exist, which cannot be explained by chronological age, but rather physiological age decline initiated even at young age due to lifestyle. At the heart of this lies the metabolic system and how this is regulated in each individual. Metabolic turnover of food to energy leads to accumulation of co-factors, byproducts, and certain proteins, which all influence gene expression through epigenetic regulation. How these epigenetic markers accumulate over time is now being investigated as the possible link between aging and many diseases, such as cancer. The relationship between metabolism and cancer was described as early as the late 1950s by Dr. Otto Warburg, before the identification of DNA and much earlier than our knowledge of epigenetics. However, when the stepwise gene mutation theory of cancer was presented, Warburg’s theories garnered little attention. Only in the last decade, with epigenetic discoveries, have Warburg’s data on the metabolic shift in cancers been brought back to life. The stepwise gene mutation theory fails to explain why large animals with more cells, do not have a greater cancer incidence than humans, known as Peto’s paradox. The resurgence of research into the Warburg effect has given us insight to what may explain Peto’s paradox. In this review, we discuss these connections and how age-related changes in metabolism are tightly linked to cancer development, which is further affected by lifestyle choices modulating the risk of aging and cancer through epigenetic control.

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    Ovarian Cancer Management in the Oldest Old: Improving Outcomes and Tailoring Treatments
    Lucia Tortorella,Giuseppe Vizzielli,Domenico Fusco,William C. Cho,Roberto Bernabei,Giovanni Scambia,Giuseppe Colloca
    A&D. 2017, 8 (5): 677-684.   DOI: 10.14336/AD.2017.0607
    Abstract   HTML   PDF (854KB) ( 52 )

    Ovarian cancer is the most common cause of death from gynecological cancers in developed countries. It is a common disease of older women at or above 63 years upon diagnosis. Thanks to advance in new treatments, mortality from ovarian cancer has declined in developed countries in the last decade. This decline in mortality rate is unevenly distributed across the age-spectrum. While mortality in younger women has decreased 21.7%, for elderly women it has declined only 2.2%. Even if ovarian cancer is clearly a disease of the elderly, older women are underrepresented in clinical trials, and scant evidence exists for the treatment of women older than 80 years. Moreover, older women are frequently undertreated, receive less chemotherapy and less combination of surgery and chemotherapy, despite the fact that this is considered the optimal treatment modality. This may be mainly due to the lack of evidence and physician’s confidence in the management of elderly women with ovarian cancer. In this review, we focus on the management of older women with ovarian cancer, considering geriatric features tied to this population.

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    Molecular Connections of Aging and Cancer
    William C. Cho
    A&D. 2017, 8 (5): 685-687.   DOI: 10.14336/AD.2017.0822
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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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