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Authors: Griñán-Ferré, Christian | Corpas, Rubén | Puigoriol-Illamola, Dolors | Palomera-Ávalos, Verónica | Sanfeliu, Coral | Pallàs, Mercè

Article Type: Review Article

Abstract: Epigenetics is emerging as the missing link among genetic inheritance, environmental influences, and body and brain health status. In the brain, specific changes in nucleic acids or their associated proteins in neurons and glial cells might imprint differential patterns of gene activation that will favor either cognitive enhancement or cognitive loss for more than one generation. Furthermore, derangement of age-related epigenetic signaling is appearing as a significant risk factor for illnesses of aging, including neurodegeneration and Alzheimer’s disease (AD). In addition, better knowledge of epigenetic mechanisms might provide hints and clues in the triggering and progression of AD. Intense research …in experimental models suggests that molecular interventions for modulating epigenetic mechanisms might have therapeutic applications to promote cognitive maintenance through an advanced age. The SAMP8 mouse is a senescence model with AD traits in which the study of epigenetic alterations may unveil epigenetic therapies against the AD. Show more

Keywords: Aging, DNA methylation, epigenetics, histone modification, neurodegeneration

DOI: 10.3233/JAD-170664

Citation: Journal of Alzheimer's Disease, vol. 62, no. 3, pp. 943-963, 2018

Authors: Porquet, David | Griñán-Ferré, Christian | Ferrer, Isidre | Camins, Antoni | Sanfeliu, Coral | del Valle, Jaume | Pallàs, Mercè

Article Type: Research Article

Abstract: The amyloid-β protein precursor/presenilin 1 (AβPP/PS1) mouse model of Alzheimer's disease (AD) has provided robust neuropathological hallmarks of familial AD-like pattern. AD is a neurodegenerative process that causes severe cognitive impairment; it is characterized by the accumulation of amyloid-β (Aβ) and hyperphosphorylated tau forms and by oxidative and inflammatory processes in brain. Currently, efforts are made to understand biochemical pathways because there is no effective therapy for AD. Resveratrol is a polyphenol that induces expression and activation of several neuroprotective pathways involving Sirtuin1 and AMPK. The objective of this work was to assess the effect of oral resveratrol administration on …AβPP/PS1 mice. Long-term resveratrol treatment significantly prevented memory loss as measured by the object recognition test. Moreover, resveratrol reduced the amyloid burden and increased mitochondrial complex IV protein levels in mouse brain. These protective effects of resveratrol were mainly mediated by increased activation of Sirtuin 1 and AMPK pathways in mice. However, an increase has been observed in IL1β and TNF gene expression, indicating that resveratrol promoted changes in inflammatory processes, although no changes were detected in other key actors of the oxidative stress pathway. Taken together, our findings suggest that resveratrol is able to reduce the harmful process that occurs in AβPP/PS1 mouse hippocampus, preventing memory loss. Show more

Keywords: AMPK, inflammation, mitochondria, resveratrol, sirtuin 1

DOI: 10.3233/JAD-140444

Citation: Journal of Alzheimer's Disease, vol. 42, no. 4, pp. 1209-1220, 2014

Authors: García-Mesa, Yoelvis | López-Ramos, Juan Carlos | Giménez-Llort, Lydia | Revilla, Susana | Guerra, Rafael | Gruart, Agnès | LaFerla, Frank M. | Cristòfol, Rosa | Delgado-García, José M. | Sanfeliu, Coral

Article Type: Research Article

Abstract: Physical exercise is considered to exert a positive neurophysiological effect that helps to maintain normal brain activity in the elderly. Expectations that it could help to fight Alzheimer's disease (AD) were recently raised. This study analyzed the effects of different patterns of physical exercise on the 3xTg-AD mouse. Male and female 3xTg-AD mice at an early pathological stage (4-month-old) have had free access to a running wheel for 1 month, whereas mice at a moderate pathological stage (7-month-old) have had access either during 1 or 6 months. The non-transgenic mouse strain was used as a control. Parallel animal groups were …housed in conventional conditions. Cognitive loss and behavioral and psychological symptoms of dementia (BPSD)-like behaviors were present in the 3xTg-AD mice along with alteration in synaptic function and ong-term potentiation impairment in vivo. Brain tissue showed AD-pathology and oxidative-related changes. Disturbances were more severe at the older age tested. Oxidative stress was higher in males but other changes were similar or higher in females. Exercise treatment ameliorated cognitive deterioration and BPSD-like behaviors such as anxiety and the startle response. Synaptic changes were partially protected by exercise. Oxidative stress was reduced. The best neuroprotection was generally obtained after 6 months of exercise in 7-month-old 3xTg-AD mice. Improved sensorimotor function and brain tissue antioxidant defence were induced in both 3xTg-AD and NonTg mice. Therefore, the benefits of aerobic physical exercise on synapse, redox homeostasis, and general brain function demonstrated in the 3xTg-AD mouse further support the value of this healthy life-style against neurodegeneration. Show more

Keywords: 3xTg-AD mouse, age, Alzheimer's disease, amyloid-β, behavior, cognition, electrophysiology, gender, oxidative stress, PHF-tau, voluntary exercise

DOI: 10.3233/JAD-2011-101635

Citation: Journal of Alzheimer's Disease, vol. 24, no. 3, pp. 421-454, 2011

Authors: García-Matas, Silvia | de Vera, Núria | Aznar, Arantxa Ortega | Marimon, Josep M. | Adell, Albert | Planas, Anna M. | Cristòfol, Rosa | Sanfeliu, Coral

Article Type: Research Article

Abstract: Alzheimer's disease (AD) is a devastating age-related neurodegenerative disease. Age is the main risk factor for sporadic AD, which is the most prevalent type. Amyloid-β peptide (Aβ) neurotoxicity is the proposed first step in a cascade of deleterious events leading to AD pathology and dementia. Glial cells play an important role in these changes. Astrocytes provide vital support to neurons and modulate functional synapses. Therefore, the toxic effects of Aβ on astrocytes might promote neurodegenerative changes that lead to AD. Aging reduces astrocyte antioxidant defenses and induces oxidative stress. We studied the effects of Aβ42 on cultures of human astrocytes …in the presence or absence of the following pro-oxidant agents: buthionine sulfoximine (BSO), a glutathione synthesis inhibitor, and FeSO4 , which liberates redox active iron. Pro-oxidant conditions potentiated Aβ toxicity, as shown by the generation of free radicals, inflammatory changes, and apoptosis. Similar treatments were assessed in rats in vivo. A combination of Aβ40 and Aβ42 or Aβ42 alone was infused intracerebroventricularly for 4 weeks. Other animal groups were also infused with BSO and FeSO4 . A long-term analysis that ended 4 months later showed greater cognitive impairment in the Morris water maze task, which was induced by Aβ plus pro-oxidant agent treatments. Pro-oxidant agents also potentiated brain tissue pathology. This was demonstrated in histological studies that showed highly increased astrocyte reactivity in AD-vulnerable areas, Aβ deposits, and oxidative damage of AD-sensitive hippocampal neurons. To increase our understanding of AD, experimental models should be used that mimic age-related brain changes, in which age-related oxidative stress potentiates the effects of Aβ. Show more

Keywords: Amyloid-β peptide, human astrocyte cultures, inflammation, iron, oxidative stress, rat model of Alzheimer's disease

DOI: 10.3233/JAD-2010-1365

Citation: Journal of Alzheimer's Disease, vol. 20, no. 1, pp. 229-245, 2010