Aging and disease

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25 March 2015. VOL 6, ISSUE 2 Previous Issue Next Issue

Conference Report

Stop Aging Disease! ICAD 2014
Stambler Ilia

2015, 6 (2): 76-94 | DOI: 10.14336/AD.2015.0115

PDF (653KB)

Review Article

Modelling the p53/p66Shc Aging Pathway in the Shortest Living Vertebrate Nothobranchius Furzeri
Chiara Priami, Giulia De Michele, Franco Cotelli, Alessandro Cellerino, Marco Giorgio, Pier Giuseppe Pelicci, Enrica Migliaccio

2015, 6 (2): 95-108 | DOI: 10.14336/AD.2014.0228

PDF (757KB)
Metabolic Syndrome, Aging and Involvement of Oxidative Stress
Francesca Bonomini, Luigi Fabrizio Rodella, Rita Rezzani

2015, 6 (2): 109-120 | DOI: 10.14336/AD.2014.0305

PDF (571KB)
Suicide in the Global Chinese Aging Population: A Review of Risk and Protective Factors, Consequences, and Interventions
XinQi Dong, E-Shien Chang, Ping Zeng, Melissa A. Simon

2015, 6 (2): 121-130 | DOI: 10.14336/AD.2014.0223

PDF (729KB)
The Role of the Tripartite Glutamatergic Synapse in the Pathophysiology of Alzheimer’s Disease
Carolyn C. Rudy, Holly C. Hunsberger, Daniel S. Weitzner, Miranda N. Reed

2015, 6 (2): 131-148 | DOI: 10.14336/AD.2014.0423

PDF (915KB)
Laparoscopic Surgery in the Elderly: A Review of the Literature
Andrew T. Bates, Celia Divino

2015, 6 (2): 149-155 | DOI: 10.14336/AD.2014.0429

PDF (541KB)
Hypoglycemia in Older People - A Less Well Recognized Risk Factor for Frailty
Ahmed H Abdelhafiz, Leocadio Rodríguez-Mañas, John E. Morley, Alan J Sinclair

2015, 6 (2): 156-167 | DOI: 10.14336/AD.2014.0330

PDF (698KB)

Cover Illustration

25 March 2015. Vol.6 No.2
Aβ-mediated increases in extracellular glutamate and the resulting excitotoxicity. (1) Aβ increases presynaptic release of glutamate. (2) Aβ elevates astrocytic calcium via stimulation of astrocytic α7 nicotinic receptors, resulting in astrocytic glutamate release via an unknown mechanism. (3) Aβ decreases glutamate clearance from the synapse, thereby prolonging the duration of glutamate in the synapse and potentially resulting in the spread of glutamate to neighboring synapses. (4) Prolonged activation of S-NMDARs and AMPARs resulting from increased extracellular glutamate is predicted to cause desensitization and internalization of NMDA/AMPA, resulting in synaptic depression. (5) Glutamate spillover activates E-NMDARs, resulting in multiple deleterious downstream events, including an increase in tau kinase activity, cell death, and blockade of long-term potentiation (LTP) and CREB phosphorylation (pCREB).

[Detail]

Cover Illustration

Aβ-mediated increases in extracellular glutamate and the resulting excitotoxicity. (1) Aβ increases presynaptic release of glutamate. (2) Aβ elevates astrocytic calcium via stimulation of astrocytic α7 nicotinic receptors, resulting in astrocytic glutamate release via an unknown mechanism. (3) Aβ decreases glutamate clearance from the synapse, thereby prolonging the duration of glutamate in the synapse and potentially resulting in the spread of glutamate to neighboring synapses. (4) Prolonged activation of S-NMDARs and AMPARs resulting from increased extracellular glutamate is predicted to cause desensitization and internalization of NMDA/AMPA, resulting in synaptic depression. (5) Glutamate spillover activates E-NMDARs, resulting in multiple deleterious downstream events, including an increase in tau kinase activity, cell death, and blockade of long-term potentiation (LTP) and CREB phosphorylation (pCREB).