Oxidative Stress in Neurodegenerative Diseases

Niedzielska, Ewa; Smaga, Irena; Gawlik, Maciej; Moniczewski, Andrzej; Stankowicz, Piotr; Pera, Joanna; Filip, Małgorzata

doi:10.1007/s12035-015-9337-5

Cited by 621 publications

(447 citation statements)

References 271 publications

Supporting

Mentioning

439

Contrasting

Unclassified

Order By: Relevance

“…Oxidative stress is generally recognized as a common feature of both acute diseases (like ischemia-induced damages) [25,32] and chronic degenerative diseases, including neurodegeneration [33], diabetes [34] and cardiovascular diseases [35], as well as cancer [18,36] and normal aging [37]. Importantly, since Nrf2 activity plays a pivotal role in redox homeostasis, its fine regulation is fundamental to counteract redox related damages.…”

Section: Nrf2 As Regulator Of Redox Homeostasismentioning

confidence: 99%

Nrf2 Pathway in Age-Related Neurological Disorders: Insights into MicroRNAs

Paladino

Conte

Caggiano

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

A general hallmark of neurological diseases is the loss of redox homeostasis that triggers oxidative damages to biomolecules compromising neuronal function. Under physiological conditions the steady-state concentrations of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are finely regulated for proper cellular functions. Reduced surveillance of endogenous antioxidant defenses and/or increased ROS/RNS production leads to oxidative stress with consequent alteration of physiological processes. Neuronal cells are particularly susceptible to ROS/RNS due to their biochemical composition. Overwhelming evidences indicate that nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-linked pathways are involved in protective mechanisms against oxidative stress by regulating antioxidant and phase II detoxifying genes. As such, Nrf2 deregulation has been linked to both aging and pathogenesis of many human chronic diseases, including neurodegenerative ones such as Parkinson’s disease, Alzheimer’s disease and amyotrophic lateral sclerosis. Nrf2 activity is tightly regulated by a fine balance between positive and negative modulators. A better understanding of the regulatory mechanisms underlying Nrf2 activity could help to develop novel therapeutic interventions to prevent, slow down or possibly reverse various pathological states. To this end, microRNAs (miRs) are attractive candidates because they are linked to intracellular redox status being regulated and, post-transcriptionally, regulating key components of ROS/RNS pathways, including Nrf2.

show abstract

Section: Nrf2 As Regulator Of Redox Homeostasismentioning

confidence: 99%

Nrf2 Pathway in Age-Related Neurological Disorders: Insights into MicroRNAs

Paladino

Conte

Caggiano

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Oxidative stress has been thought one of the main reason that takes over a potential role in the pathogenesis of AD. Clinical and also preclinical researches show that neurodegenerative diseases such as AD are connected with higher levels of oxidative stress biomarkers and by lower levels of antioxidant defense biomarkers in the brain (24). Our study has been arised by this main topic.…”

Section: Discussionmentioning

confidence: 90%

The Effect of Apocynin on Motor and Cognitive Functions in Experimental Alzheimer’s disease

Akyuva

Önal²,

Parlakpınar³

et al. 2018

Period Biol

View full text Add to dashboard Cite

Scope: We investigated the potential beneficial effect of Apocynin (APO) on motor and cognitive functions in experimental Alzheimer's disease (AD). Materials and Methods: Experimental AD was induced in rats by Conclusion: These results indicate that APO can provide neuro-protective effect for motor but not for cognitive performance in experimental AD. INTRODUCTIONI nflammation has been shown to play a vital role in the pathophysiology of the Alzheimer's disease (AD). Microglial cells are responsible for removing the remnants of apoptotic neurons and by doing so they induce an inflammatory response against amyloid plaques via oxidative stress. This theory claims that oxidative stress is the main damaging factor in AD (1, 2, 3). However, antioxidant molecules have not shown to demonstrate significant clinical benefits (2, 4).Recent researches indicate that AD is a brain-specific form of diabetes (5, 6). Hyperglycemia and hyperinsulinemia are correlated with development of 7). Defective insulin signaling, altered levels and/or abnormal activation of components of the insulin signaling pathway, and, more importantly, decreased responsiveness to insulin were found in AD (5,8). In response to infection, trauma or abnormal collection of protein aggregates; TNF-a is produced mainly from microglial cells in the brain. TNF-a levels are increased in AD

show abstract

“…The concept that free radicals degrade DNA and proteins suggest that anti-oxidative strategies would prevent cell death. There is ample evidence of the presence of increased oxidative stress in the damaged CNS in MS, neurodegenerative diseases, stroke and epilepsy [36][37][38]. However, oxidation in mitochondria and other organelles is a complex process required for energy production and other metabolic activities (e.g.…”

Section: Neuroprotective Strategiesmentioning

confidence: 99%

Neuroprotective therapies for multiple sclerosis and other demyelinating diseases

Villoslada

2016

Mult Scler Demyelinating Disord

View full text Add to dashboard Cite

Damage to the Central Nervous Systems (CNS) in Multiple Sclerosis (MS) seems to be mainly due to chronic inflammation of the CNS with superimposed bouts of inflammatory activity by the adaptive immune system. The immune mediated damage can be amplified by neurodegenerative mechanisms in damaged axons including anterograde or retrograde axonal or transynaptic degeneration, synaptic pruning and neuronal or oligodendrocyte death. As such, it is highly unlikely that CNS damage can be prevented using only immunomodulatory drugs. For this reason, neuroprotection, aimed at preventing axonal, neuronal, myelin, and oligodendrocyte damage and cell death in the presence of this toxic microenvironment is highly pursued in MS and other demyelinating diseases. Neuroprotective strategies target different processes including oxidative stress, ionic imbalance (sodium, potassium or calcium), energy depletion, trophic factor support, metabolites balance, excitotoxicity, apoptosis, remyelination, etc. Although none of these strategies have translated into approved drugs to date, improvement in the understanding of underlying biology, in the design of clinical trials specific for assessing neuroprotection, and new technologies for developing novel therapies for neuroprotection suggest a new avenue for treating MS, Optic Neuritis or Neuromyelitis Optica (NMO). Several of these therapies are now entering clinical phases and if successful, such strategies would improve patients' quality of life, and will be even more critical for patients with progressive MS. In the event that such therapies target natural repair mechanisms rather than disease specific processes, they can potentially be useful for other brain diseases such as stroke, neurodegenerative diseases, brain trauma or epilepsy.

show abstract

Oxidative Stress in Neurodegenerative Diseases

Cited by 621 publications

References 271 publications

Nrf2 Pathway in Age-Related Neurological Disorders: Insights into MicroRNAs

Nrf2 Pathway in Age-Related Neurological Disorders: Insights into MicroRNAs

The Effect of Apocynin on Motor and Cognitive Functions in Experimental Alzheimer’s disease

Neuroprotective therapies for multiple sclerosis and other demyelinating diseases

Contact Info

Product

Resources

About