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Cover Illustration
2015, Vol.6  No.5
Oxidative stress and Neurotoxicity. A. Shows the neurotoxic mechanisms of DA and neurotoxins used to mimic PD in the dopaminergic neuron. DA and the neurotoxins 6-hydroxydopmine (6-OHDA) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), cause reactive species of oxygen (ROS) affecting the mitochondrial function and lipopeMPTP is first incorporated into the glial cells and metabolized to MPP+, this metabolite can cross the membrane through the DA transporter (DAT) to reach intracellular compartments in DAergic neuron, while 6-OHDA can directly cross through DAT. B. Neurotoxicity by renin-angiotensin system (RAS) activation and DA receptors. In RAS, angiotensinogen is converted to Angiotensin I (AI) by renin, AI is converted into Angiotensin II (AII) thought angiotensin converting enzyme (ACE), AII mediate their actions by angiotensin receptors AT1 and AT2Rs. AT1Rs activate the nicotidamine adenine dinucleotide phosphate oxidase complex (NADPH), which is the major source of ROS causing mitochondrial dysfunction and inflammatory response. The interaction AT1Rs with of D1 and D3Rs increases the DA response while D5Rs can regulate the AT1Rs by proteasome mechanisms. DA receptors are also related with immune response in T cells. [Detail] ...

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  • Table of Content
      01 October 2015, Volume 6 Issue 5 Previous Issue    Next Issue
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    GUEST EDITOR INSTRODUCTION
    GUEST EDITOR INSTRODUCTION
    Aging and disease. 2015, 6 (5): 1-01.  
    Abstract   HTML   PDF (127KB) ( 200 )
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    Mini-review
    Possible Benefit of Dietary Carnosine towards Depressive Disorders
    Alan R. Hipkiss*
    Aging and disease. 2015, 6 (5): 300-303.   DOI: 10.14336/AD.2014.1211
    Abstract   HTML   PDF (489KB) ( 1893 )

    Many stress-related and depressive disorders have been shown to be associated with one or more of the following; shortened telomeres, raised cortisol levels and increased susceptibility to age-related dysfunction. It is suggested here that insufficient availability of the neurological peptide, carnosine, may provide a biochemical link between stress- and depression-associated phenomena: there is evidence that carnosine can enhance cortisol metabolism, suppress telomere shortening and exert anti-aging activity in model systems. Dietary supplementation with carnosine has been shown to suppress stress in animals, and improve behaviour, cognition and well-being in human subjects. It is therefore proposed that the therapeutic potential of carnosine dietary supplementation towards stress-related and depressive disorders should be examined.

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    Review Article
    Metabolic Alterations Associated to Brain Dysfunction in Diabetes
    João M. N. Duarte
    Aging and disease. 2015, 6 (5): 304-321.   DOI: 10.14336/AD.2014.1104
    Abstract   HTML   PDF (733KB) ( 1742 )

    From epidemiological studies it is known that diabetes patients display increased risk of developing dementia. Moreover, cognitive impairment and Alzheimer’s disease (AD) are also accompanied by impaired glucose homeostasis and insulin signalling. Although there is plenty of evidence for a connection between insulin-resistant diabetes and AD, definitive linking mechanisms remain elusive. Cerebrovascular complications of diabetes, alterations in glucose homeostasis and insulin signalling, as well as recurrent hypoglycaemia are the factors that most likely affect brain function and structure. While difficult to study in patients, the mechanisms by which diabetes leads to brain dysfunction have been investigated in experimental models that display phenotypes of the disease. The present article reviews the impact of diabetes and AD on brain structure and function, and discusses recent findings from translational studies in animal models that link insulin resistance to metabolic alterations that underlie brain dysfunction. Such modifications of brain metabolism are likely to occur at early stages of neurodegeneration and impact regional neurochemical profiles and constitute non-invasive biomarkers detectable by magnetic resonance spectroscopy (MRS).

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    SUMOylation: Novel Neuroprotective Approach for Alzheimer’s Disease?
    Juliana B. Hoppe, Christianne G. Salbego, Helena Cimarosti
    Aging and disease. 2015, 6 (5): 322-330.   DOI: 10.14336/AD.2014.1205
    Abstract   HTML   PDF (711KB) ( 1153 )

    Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized in the brain by the formation of amyloid-beta (Aβ)-containing plaques and neurofibrillary tangles containing the microtubule-associated protein tau. Neuroin?ammation is another feature of AD and astrocytes are receiving increasing attention as key contributors. Although some progress has been made, the molecular mechanisms underlying the pathophysiology of AD remain unclear. Interestingly, some of the main proteins involved in AD, including amyloid precursor protein (APP) and tau, have recently been shown to be SUMOylated. The post-translational modification by SUMO (small ubiquitin-like modifier) has been shown to regulate APP and tau and may modulate other proteins implicated in AD. Here we present an overview of recent studies suggesting that protein SUMOylation might be involved in the underlying pathogenic mechanisms of AD and discuss how this could be exploited for therapeutic intervention.

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    The involvement of BDNF, NGF and GDNF in aging and Alzheimer's disease
    Josiane Budni, Tatiani Bellettini-Santos, Francielle Mina, Michelle Lima Garcez, Alexandra Ioppi Zugno
    Aging and disease. 2015, 6 (5): 331-341.   DOI: 10.14336/AD.2015.0825
    Abstract   HTML   PDF (849KB) ( 1874 )

    Aging is a normal physiological process accompanied by cognitive decline. This aging process has been the primary risk factor for development of aging-related diseases such as Alzheimer's disease (AD). Cognitive deficit is related to alterations of neurotrophic factors level such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and glial cell-derived neurotrophic factor (GDNF). These strong relationship between aging and AD is important to investigate the time which they overlap, as well as, the pathophysiological mechanism in each event. Considering that aging and AD are related to cognitive impairment, here we discuss the involving these neurotrophic factors in the aging process and AD.

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    Does Infection-Induced Immune Activation Contribute to Dementia?
    Tatiana Barichello, Jaqueline S. Generoso, Jessica A. Goularte, Allan Collodel, Meagan R. Pitcher, Lutiana R. Simões, João Quevedo, Felipe Dal-Pizzol
    Aging and disease. 2015, 6 (5): 342-348.   DOI: 10.14336/AD.2015.0521
    Abstract   HTML   PDF (1010KB) ( 1365 )

    The central nervous system (CNS) is protected by a complex blood-brain barrier system; however, a broad diversity of virus, bacteria, fungi, and protozoa can gain access and cause illness. As pathogens replicate, they release molecules that can be recognized by innate immune cells. These molecules are pathogen-associated molecular patterns (PAMP) and they are identified by pattern-recognition receptors (PRR) expressed on antigen-presenting cells. Examples of PRR include toll-like receptors (TLR), receptors for advanced glycation endproducts (RAGE), nucleotide binding oligomerisation domain (NOD)-like receptors (NLR), c-type lectin receptors (CLR), RIG-I-like receptors (RLR), and intra-cytosolic DNA sensors. The reciprocal action between PAMP and PRR triggers the release of inflammatory mediators that regulate the elimination of invasive pathogens. Damage-associated molecular patterns (DAMP) are endogenous constituents released from damaged cells that also have the ability to activate the innate immune response. An increase of RAGE expression levels on neurons, astrocytes, microglia, and endothelial cells could be responsible for the accumulation of αβ-amyloid in dementia and related to the chronic inflammatory state that is found in neurodegenerative disorders.

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    Dopamine Receptors and Neurodegeneration
    Claudia Rangel-Barajas, Israel Coronel, Benjamín Florán
    Aging and disease. 2015, 6 (5): 349-368.   DOI: 10.14336/AD.2015.0330
    Abstract   HTML   PDF (1415KB) ( 1937 )

    Dopamine (DA) is one of the major neurotransmitters and participates in a number of functions such as motor coordination, emotions, memory, reward mechanism, neuroendocrine regulation etc. DA exerts its effects through five DA receptors that are subdivided in 2 families: D1-like DA receptors (D1 and D5) and the D2-like (D2, D3 and D4). All DA receptors are widely expressed in the central nervous system (CNS) and play an important role in not only in physiological conditions but also pathological scenarios. Abnormalities in the DAergic system and its receptors in the basal ganglia structures are the basis Parkinson’s disease (PD), however DA also participates in other neurodegenerative disorders such as Huntington disease (HD) and multiple sclerosis (MS). Under pathological conditions reorganization of DAergic system has been observed and most of the times, those changes occur as a mechanism of compensation, but in some cases contributes to worsening the alterations. Here we review the changes that occur on DA transmission and DA receptors (DARs) at both levels expression and signals transduction pathways as a result of neurotoxicity, inflammation and in neurodegenerative processes. The better understanding of the role of DA receptors in neuropathological conditions is crucial for development of novel therapeutic approaches to treat alterations related to neurodegenerative diseases.

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    Carnosine and Related Peptides: Therapeutic Potential in Age-Related Disorders
    José H. Cararo, Emilio L. Streck, Patricia F. Schuck, Gustavo da C. Ferreira
    Aging and disease. 2015, 6 (5): 369-379.   DOI: 10.14336/AD.2015.0616
    Abstract   HTML   PDF (879KB) ( 1011 )

    Imidazole dipeptides (ID), such as carnosine (β-alanyl-L-histidine), are compounds widely distributed in excitable tissues of vertebrates. ID are also endowed of several biochemical properties in biological tissues, including antioxidant, bivalent metal ion chelating, proton buffering, and carbonyl scavenger activities. Furthermore, remarkable biological effects have been assigned to such compounds in age-related human disorders and in patients whose activity of serum carnosinase is deficient or undetectable. Nevertheless, the precise biological role of ID is still to be unraveled. In the present review we shall discuss some evidences from clinical and basic studies for the utilization of ID as a drug therapy for age-related human disorders.

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    Mechanisms of Muscle Denervation in Aging: Insights from a Mouse Model of Amyotrophic Lateral Sclerosis
    Kevin H.J. Park
    Aging and disease. 2015, 6 (5): 380-389.   DOI: 10.14336/AD.2015.0506
    Abstract   HTML   PDF (609KB) ( 928 )

    Muscle denervation at the neuromuscular junction (NMJ) is thought to be a contributing factor in age-related muscle weakness. Therefore, understanding the mechanisms that modulate NMJ innervation is a key to developing therapies to combat age-related muscle weakness affecting the elderly. Two mouse models, one lacking the Cu/Zn superoxide dismutase (SOD1) gene and another harboring the transgenic mutant human SOD1 gene, display progressive changes at the NMJ, including muscle endplate fragmentation, nerve terminal sprouting, and denervation. These changes at the NMJ share many of the common features observed in the NMJs of aged mice. In this review, research findings demonstrating the effects of PGC-1α, IGF-1, GDNF, MyoD, myogenin, and miR-206 on NMJ innervation patterns in the G93A SOD1 mice will be highlighted in the context of age-related muscle denervation.

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    Phenylketonuria Pathophysiology: on the Role of Metabolic Alterations
    Patrícia Fernanda Schuck, Fernanda Malgarin, José Henrique Cararo, Fabiola Cardoso, Emilio Luiz Streck, Gustavo Costa Ferreira
    Aging and disease. 2015, 6 (5): 390-399.   DOI: 10.14336/AD.2015.0827
    Abstract   HTML   PDF (874KB) ( 1938 )

    Phenylketonuria (PKU) is an inborn error of phenylalanine (Phe) metabolism caused by the deficiency of phenylalanine hydroxylase. This deficiency leads to the accumulation of Phe and its metabolites in tissues and body fluids of PKU patients. The main signs and symptoms are found in the brain but the pathophysiology of this disease is not well understood. In this context, metabolic alterations such as oxidative stress, mitochondrial dysfunction, and impaired protein and neurotransmitters synthesis have been described both in animal models and patients. This review aims to discuss the main metabolic disturbances reported in PKU and relate them with the pathophysiology of this disease. The elucidation of the pathophysiology of brain damage found in PKU patients will help to develop better therapeutic strategies to improve quality of life of patients affected by this condition.

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    Potential Therapeutical Contributions of the Endocannabinoid System towards Aging and Alzheimer’s Disease
    Amandine E. Bonnet, Yannick Marchalant
    Aging and disease. 2015, 6 (5): 400-405.   DOI: 10.14336/AD.2015.0617
    Abstract   HTML   PDF (636KB) ( 1995 )

    Aging can lead to decline in cognition, notably due to neurodegenerative processes overwhelming the brain over time. As people live longer, numerous concerns are rightfully raised toward long-term slowly incapacitating diseases with no cure, such as Alzheimer’s disease. Since the early 2000’s, the role of neuroinflammation has been scrutinized for its potential role in the development of diverse neurodegenerative diseases notably because of its slow onset and chronic nature in aging. Despite the lack of success yet, treatment of chronic neuroinflammation could help alleviate process implicated in neurodegenerative disease. A growing number of studies including our own have aimed at the endocannabinoid system and unfolded unique effects of this system on neuroinflammation, neurogenesis and hallmarks of Alzheimer’s disease and made it a reasonable target in the context of normal and pathological brain aging.

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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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