Mitochondria and Alzheimer's disease

Piaceri, Irene; Rinnoci, Valentina; Bagnoli, Silvia; Failli, Ylenia; Sorbi, Sandro

doi:10.1016/j.jns.2012.05.033

Cited by 35 publications

(23 citation statements)

References 61 publications

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“…Patients presenting with neurological disorders, for example, AD, PD, and Gulf War Illness (GWI), are burdened with a significant number of dysfunctional mitochondria [Federico et al, 2012;Piaceri et al, 2012;Swerdlow, 2012;Chaturvedi and Beal, 2013;Wallace, 2013;Forbes-Hernandez et al, 2014;Nicolson et al, 2014;Pagano et al, 2014;Sodhi et al, 2014;Weisfeld-Adams et al, 2015;Woo et al, 2015]. Mitophagy [Novak, 2012;Ashrafi and Schwarz, 2013;Gomes and Scorrano, 2013;Morris et al, 2014;Pinho et al, 2014;Pinto and Moraes, 2014], a selective subform of autophagy [Choi et al, 2013;Schneider and Cuervo, 2014], is a cellular mechanism for removing dysfunctional mitochondria mediated by PINK1 and PARK2 genes working together Kane and Youle, 2012;Youle and van der Bliek, 2012;Allen et al, 2013;Ashrafi and Schwarz, 2013;Trempe et al, 2013;Redmann et al, 2014;Frake et al, 2015;Pickrell and Youle, 2015].…”

Section: Apoptotic Priming In Mitochondriamentioning

confidence: 99%

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Irwin

Moos

Faller

et al. 2016

Drug Development Research

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Preclinical Research In this review, we discuss epigenetic-driven methods for treating neurodegenerative disorders associated with mitochondrial dysfunction, focusing on carnitinoid antioxidant-histone deacetylase inhibitors that show an ability to reinvigorate synaptic plasticity and protect against neuromotor decline in vivo. Aging remains a major risk factor in patients who progress to dementia, a clinical syndrome typified by decreased mental capacity, including impairments in memory, language skills, and executive function. Energy metabolism and mitochondrial dysfunction are viewed as determinants in the aging process that may afford therapeutic targets for a host of disease conditions, the brain being primary in such thinking. Mitochondrial dysfunction is a core feature in the pathophysiology of both Alzheimer and Parkinson diseases and rare mitochondrial diseases. The potential of new therapies in this area extends to glaucoma and other ophthalmic disorders, migraine, Creutzfeldt-Jakob disease, post-traumatic stress disorder, systemic exertion intolerance disease, and chemotherapy-induced cognitive impairment. An emerging and hopefully more promising approach to addressing these hard-to-treat diseases leverages their sensitivity to activation of master regulators of antioxidant and cytoprotective genes, antioxidant response elements, and mitophagy. Drug Dev Res 77 : 109-123, 2016. © 2016 Wiley Periodicals, Inc.

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Section: Apoptotic Priming In Mitochondriamentioning

confidence: 99%

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Irwin

Moos

Faller

et al. 2016

Drug Development Research

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“…Mitochondrial dysfunction is now generally accepted as a general pathological feature in AD patients (Mattson et al , 2008; Piaceri et al , 2012; Selfridge et al , 2013). In line with this, a modification of the amyloid cascade hypothesis was postulated that supports the correlation between mitochondrial dysfunction with AD.…”

Section: Introductionmentioning

confidence: 99%

Amyloid β-peptides interfere with mitochondrial preprotein import competence by a coaggregation process

Cenini

Rüb

Bruderek

et al. 2016

MBoC

103

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“…Our results showed that xanthoceraside could significantly attenuate the ATP depletion in the cerebral cortex and hippocampus compared with model mice induced by A β 1-42, improving the mitochondrial dysfunction. Some studies reported that the interaction between A β and ATP synthesis may result in ATP deletion [44]. Furthermore, a subsequent study reported that A β could decrease the activity of cytochrome c oxidase (COX) and inhibit the mitochondrial respiratory function, finally, leading to the ATP deletion and ROS overproduction.…”

Section: Discussionmentioning

confidence: 99%

Xanthoceraside Ameliorates Mitochondrial Dysfunction Contributing to the Improvement of Learning and Memory Impairment in Mice with Intracerebroventricular Injection of Aβ1‐42

Chi

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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The effects of xanthoceraside on learning and memory impairment were investigated and the possible mechanism associated with the protection of mitochondria was also preliminarily explored in Alzheimer's disease (AD) mice model induced by intracerebroventricular (i.c.v.) injection of Aβ1-42. The results indicated that xanthoceraside (0.08–0.32 mg/kg) significantly improved learning and memory impairment in Morris water maze test and Y-maze test. Xanthoceraside significantly reversed the aberrant decrease of ATP levels and attenuated the abnormal increase of ROS levels both in the cerebral cortex and hippocampus in mice injected with Aβ1-42. Moreover, xanthoceraside dose dependently reversed the decrease of COX, PDHC, and KGDHC activity in isolated cerebral cortex mitochondria of the mice compared with Aβ1-42 injected model mice. In conclusion, xanthoceraside could improve learning and memory impairment, promote the function of mitochondria, decrease the production of ROS, and inhibit oxidative stress. The improvement effects on mitochondria may be through withstanding the damage of Aβ to mitochondrial respiratory chain and the key enzymes in Kreb's cycle. Therefore, the results from present study and previous study indicate that xanthoceraside could be a competitive candidate for the treatment of AD.

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Mitochondria and Alzheimer's disease

Cited by 35 publications

References 61 publications

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Epigenetic Treatment of Neurodegenerative Disorders: Alzheimer and Parkinson Diseases

Amyloid β-peptides interfere with mitochondrial preprotein import competence by a coaggregation process

Xanthoceraside Ameliorates Mitochondrial Dysfunction Contributing to the Improvement of Learning and Memory Impairment in Mice with Intracerebroventricular Injection of Aβ1‐42

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