Aging and disease

ISOAD Become a Member Search

X

Advanced Search

Table of Content

01 October 2015. VOL 6, ISSUE 5 Previous Issue Next Issue

Review Article

Metabolic Alterations Associated to Brain Dysfunction in Diabetes

2015, 6 (5): 304-321 | DOI: 10.14336/AD.2014.1104

PDF (733KB)
SUMOylation: Novel Neuroprotective Approach for Alzheimer’s Disease?

2015, 6 (5): 322-330 | DOI: 10.14336/AD.2014.1205

PDF (711KB)

Mini-review

Possible Benefit of Dietary Carnosine towards Depressive Disorders

2015, 6 (5): 300-303 | DOI: 10.14336/AD.2014.1211

PDF (489KB)

Review Article

Dopamine Receptors and Neurodegeneration

2015, 6 (5): 349-368 | DOI: 10.14336/AD.2015.0330

PDF (1415KB)
Mechanisms of Muscle Denervation in Aging: Insights from a Mouse Model of Amyotrophic Lateral Sclerosis

2015, 6 (5): 380-389 | DOI: 10.14336/AD.2015.0506

PDF (609KB)
Does Infection-Induced Immune Activation Contribute to Dementia?

2015, 6 (5): 342-348 | DOI: 10.14336/AD.2015.0521

PDF (1010KB)
Potential Therapeutical Contributions of the Endocannabinoid System towards Aging and Alzheimer’s Disease

2015, 6 (5): 400-405 | DOI: 10.14336/AD.2015.0617

PDF (636KB)
Carnosine and Related Peptides: Therapeutic Potential in Age-Related Disorders

2015, 6 (5): 369-379 | DOI: 10.14336/AD.2015.0616

PDF (879KB)
The involvement of BDNF, NGF and GDNF in aging and Alzheimer's disease

2015, 6 (5): 331-341 | DOI: 10.14336/AD.2015.0825

PDF (849KB)

GUEST EDITOR INSTRODUCTION

GUEST EDITOR INSTRODUCTION

2015, 6 (5): 1-01

PDF (127KB)

Review Article

Phenylketonuria Pathophysiology: on the Role of Metabolic Alterations

2015, 6 (5): 390-399 | DOI: 10.14336/AD.2015.0827

PDF (874KB)

Cover Illustration

01 October 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 lipoperoxidation and cytoskeletal disorganization, which leads energy crisis and neuronal death. MPTP 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]

Cover Illustration

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 lipoperoxidation and cytoskeletal disorganization, which leads energy crisis and neuronal death. MPTP 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.