Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models – Nature Medicine — Pesquisa liderada por brasileiros aponta que hormônio pode reverter perda de memória causada pelo Alzheimer

Do the downloads!! Share!! The diffusion of very important information and knowledge is essential for the world progress always!! Thanks!!

  • – > Mestrado – Dissertation – Tabelas, Figuras e Gráficos – Tables, Figures and Graphics – ´´My´´ Dissertation @ #Innovation #energy #life #health #Countries #Time #Researches #Reference #Graphics #Ages #Age #Mice #People #Person #Mouse #Genetics #PersonalizedMedicine #Diagnosis #Prognosis #Treatment #Disease #UnknownDiseases #Future #VeryEfficientDrugs #VeryEfficientVaccines #VeryEfficientTherapeuticalSubstances #Tests #Laboratories #Investments #Details #HumanLongevity #DNA #Cell #Memory #Physiology #Nanomedicine #Nanotechnology #Biochemistry #NewMedicalDevices #GeneticEngineering #Internet #History #Science #World

Pathol Res Pract. 2012 Jul 15;208(7):377-81. doi: 10.1016/j.prp.2012.04.006. Epub 2012 Jun 8.

The influence of physical activity in the progression of experimental lung cancer in mice

Renato Batista Paceli 1Rodrigo Nunes CalCarlos Henrique Ferreira dos SantosJosé Antonio CordeiroCassiano Merussi NeivaKazuo Kawano NagaminePatrícia Maluf Cury


Impact_Fator-wise_Top100Science_Journals

GRUPO_AF1 – GROUP AFA1 – Aerobic Physical Activity – Atividade Física Aeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto

GRUPO AFAN 1 – GROUP AFAN1 – Anaerobic Physical Activity – Atividade Física Anaeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto

GRUPO_AF2 – GROUP AFA2 – Aerobic Physical Activity – Atividade Física Aeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto

GRUPO AFAN 2 – GROUP AFAN 2 – Anaerobic Physical Activity – Atividade Física Anaeróbia – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto

Slides – mestrado – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto

CARCINÓGENO DMBA EM MODELOS EXPERIMENTAIS

DMBA CARCINOGEN IN EXPERIMENTAL MODELS

Avaliação da influência da atividade física aeróbia e anaeróbia na progressão do câncer de pulmão experimental – Summary – Resumo – ´´My´´ Dissertation – Faculty of Medicine of Sao Jose do Rio Preto

https://pubmed.ncbi.nlm.nih.gov/22683274/

Abstract

Lung cancer is one of the most incident neoplasms in the world, representing the main cause of mortality for cancer. Many epidemiologic studies have suggested that physical activity may reduce the risk of lung cancer, other works evaluate the effectiveness of the use of the physical activity in the suppression, remission and reduction of the recurrence of tumors. The aim of this study was to evaluate the effects of aerobic and anaerobic physical activity in the development and the progression of lung cancer. Lung tumors were induced with a dose of 3mg of urethane/kg, in 67 male Balb – C type mice, divided in three groups: group 1_24 mice treated with urethane and without physical activity; group 2_25 mice with urethane and subjected to aerobic swimming free exercise; group 3_18 mice with urethane, subjected to anaerobic swimming exercise with gradual loading 5-20% of body weight. All the animals were sacrificed after 20 weeks, and lung lesions were analyzed. The median number of lesions (nodules and hyperplasia) was 3.0 for group 1, 2.0 for group 2 and 1.5-3 (p=0.052). When comparing only the presence or absence of lesion, there was a decrease in the number of lesions in group 3 as compared with group 1 (p=0.03) but not in relation to group 2. There were no metastases or other changes in other organs. The anaerobic physical activity, but not aerobic, diminishes the incidence of experimental lung tumors.

Hormone could slow Alzheimer’s progression 8 January 2019, by Anne Craig 2019-01-hormone-alzheimer(1) pdf

https://www.nature.com/articles/s41591-018-0275-4

https://www.ferreiralab.org/lab-team

http://www.alzheimerlabs.com

https://www.pathology.columbia.edu/profile/ottavio-arancio-md

The Role of Irisin in Alzheimer’s Disease (Important issue – Assunto importante) https://www.mdpi.com/2077-0383/7/11/407/html

http://g1.globo.com/jornal-nacional/noticia/2017/07/cientistas-da-ufrj-conseguem-parar-o-avanco-do-alzheimer-em-animais.html (Related research – Pesquisa relacionada)

https://oglobo.globo.com/sociedade/saude/cientistas-brasileiros-descobrem-como-prevenir-alzheimer-23352037

https://www.nhs.uk/news/neurology/exercise-hormone-may-play-role-combating-alzheimers-disease/

https://g1.globo.com/resumo-do-dia/noticia/2019/01/07/segunda-feira-7-de-janeiro.ghtml

http://revistapesquisa.fapesp.br/2019/01/07/hormonio-do-exercicio-pode-evitar-a-perda-de-memoria/

http://www.abc.org.br/2019/01/08/cientistas-brasileiros-descobrem-como-prevenir-alzheimer/

http://www.cliquemaranhao.com.br/

https://vaaju.com/brazil/pesquisas-sugerem-que-o-hormonio-pode-converter-perda-de-memoria/

Pesquisa liderada pelo governo brasileiro sugere que o hormônio pode reverter a perda de memória causada por Alzheimer | Ciência e Saúde

http://www.gaz.com.br/conteudos/geral/2019/01/07/137859-cientistas_brasileiros_descobrem_como_prevenir_alzheimer.html.php

https://www.mblnews.org/notas/orgulho-nacional-cientistas-brasileiros-descobrem-como-prevenir-alzheimer/

Exercício físico é a chave de cura para o Alzheimer, diz pesquisa

http://www.fmclube.com.br/noticia.php?id=2004

https://medicalxpress.com/news/2019-01-hormone-alzheimer.html

 

 

 

 

Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models

 

 

Uma nova esperança

´´Cientistas brasileiros revelaram que há relação entre um hormônio chamado irisina, produzido pelo corpo durante a prática de exercícios físicos, e o tratamento da perda da memória provocada pelo Alzheimer. O estudo, publicado na revista “Nature Medicine”, foi feito com camundongos que têm a doença. Eles foram estimulados a produzir o hormônio e também receberam doses. Os autores dizem que 3 novidades foram descobertas:´´

  • há baixos níveis de irisina no cérebro de pacientes afetados pelo Alzheimer. Essa mesma deficiência foi vista nos camundongos;
  • a reposição dos níveis de irisina no cérebro, inclusive por meio de exercícios físicos, foi capaz de reverter a perda de memória;
  • a irisina é o que regula os efeitos positivos do exercício físico na memória dos camundongos.

´´Os pesquisadores Mychael Lourenço e Fernanda De Felice, da UFRJ, explicam que o fato de a irisina ser produzida pelo próprio organismo diminui as chances de efeitos colaterais, o que dá esperança para novos tratamentos. Leia mais sobre a pesquisa.´´

LOURENCO, MYCHAEL V. ; FROZZA, RUDIMAR L. ; FREITAS, G. B. ; ZHANG, H. ; KINCHESKI, GRASIELLE C. ; CLARKE, J. R. ; RIBEIRO, FELIPE C. ; BECKMAN, DANIELLE ; STANISZEVSKI, A. ; BERMAN, H. ; GUERRA, L. A. ; FORNY-GERMANO, LETICIA ; MEIER, S. ; ABISAMBRA, J. F. ; WILCOCK, D. M. ; PRADO, M. A. M. ; DE SOUZA, JORGE M. ; ALVES-LEON, S. ; TOVAR-MOLL, F. ; MATTOS, P. ; ARANCIO, O. ; Ferreira ST. ; DE FELICE, FERNANDA G. . Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer´s models. NATURE MEDICINE , 2018.

Abstract

Defective brain hormonal signaling has been associated with Alzheimer’s disease (AD), a disorder characterized by synapse and memory failure. Irisin is an exercise-induced myokine released on cleavage of the membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5), also expressed in the hippocampus. Here we show that FNDC5/irisin levels are reduced in AD hippocampi and cerebrospinal fluid, and in experimental AD models. Knockdown of brain FNDC5/irisin impairs long-term potentiation and novel object recognition memory in mice. Conversely, boosting brain levels of FNDC5/irisin rescues synaptic plasticity and memory in AD mouse models. Peripheral overexpression of FNDC5/irisin rescues memory impairment, whereas blockade of either peripheral or brain FNDC5/irisin attenuates the neuroprotective actions of physical exercise on synaptic plasticity and memory in AD mice. By showing that FNDC5/irisin is an important mediator of the beneficial effects of exercise in AD models, our findings place FNDC5/irisin as a novel agent capable of opposing synapse failure and memory impairment in AD.

References

1.

Prince, M. et al. The global prevalence of dementia: a systematic review and metaanalysis. Alzheimers Dement. 9, 63–75.e62 (2013).

  • 2.

Ferreira, S. T., Lourenco, M. V., Oliveira, M. M. & De Felice, F. G. Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer’s disease. Front. Cell. Neurosci. 9, 191 (2015).

  • 3.

Fernandez, A. M. & Torres-Alemán, I. The many faces of insulin-like peptide signalling in the brain. Nat. Rev. Neurosci. 13, 225–239 (2012).

  • 4.

Biessels, G. J. & Reagan, L. P. Hippocampal insulin resistance and cognitive dysfunction. Nat. Rev. Neurosci. 16, 660–671 (2015).

  • 5.

McEwen, B. S. Preserving neuroplasticity: role of glucocorticoids and neurotrophins via phosphorylation. Proc. Natl Acad. Sci. USA 112, 15544–15545 (2015).

  • 6.

During, M. J. et al. Glucagon-like peptide-1 receptor is involved in learning and neuroprotection. Nat. Med. 9, 1173–1179 (2003).

  • 7.

Chiu, S.-L., Chen, C.-M. & Cline, H. T. Insulin receptor signaling regulates synapse number, dendritic plasticity, and circuit function in vivo. Neuron 58, 708–719 (2008).

  • 8.

Grillo, C. A. et al. Hippocampal insulin resistance impairs spatial learning and synaptic plasticity. Diabetes 64, 3927–3936 (2015).

  • 9.

Irving, A. J. & Harvey, J. Leptin regulation of hippocampal synaptic function in health and disease. Philos. Trans. R. Soc. Lond. B 369, 20130155 (2013).

  • 10.

Lourenco, M. V., Ferreira, S. T. & De Felice, F. G. Neuronal stress signaling and eIF2α phosphorylation as molecular links between Alzheimer’s disease and diabetes. Prog. Neurobiol. 129, 37–57 (2015).

  • 11.

Bomfim, T. R. et al. An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer’s disease-associated Aβ oligomers. J. Clin. Invest. 122, 1339–1353 (2012).

  • 12.

Talbot, K. et al. Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. J. Clin. Invest. 122, 1316–1338 (2012).

  • 13.

De Felice, F. G., Lourenco, M. V. & Ferreira, S. T. How does brain insulin resistance develop in Alzheimer’s disease? Alzheimers Dement. 10, S26–S32 (2014).

  • 14.

Wadman, M. US government sets out Alzheimer’s plan. Nature 485, 426–427 (2012).

  • 15.

De Felice, F. G. Alzheimer’s disease and insulin resistance: translating basic science into clinical applications. J. Clin. Invest. 123, 531–539 (2013).

  • 16.

Boström, P. et al. A PGC1-α-dependent myokine that drives brown-fat-like development of white fat and thermogenesis. Nature 481, 463–468 (2012).

  • 17.

Jedrychowski, M. P. et al. Detection and quantitation of circulating human irisin by tandem mass spectrometry. Cell Metab. 22, 734–740 (2015).

  • 18.

Wrann, C.D. et al. Exercise induces hippocampal BDNF through a PGC-1α/FNDC5 pathway. Cell Metab. 18, 649–659 (2013).

  • 19.

Chen, K. et al. Irisin protects mitochondria function during pulmonary ischemia/reperfusion injury. Sci. Transl. Med. 9, eaao6298 (2017).

  • 20.

Lee, P. et al. Irisin and FGF21 are cold-induced endocrine activators of brown fat function in humans. Cell Metab. 19, 302–309 (2014).

  • 21.

Schumacher, M. A., Chinnam, N., Ohashi, T., Shah, R. S. & Erickson, H. P. The structure of irisin reveals a novel intersubunit β-sheet fibronectin type III (FNIII) dimer: implications for receptor activation. J. Biol. Chem. 288, 33738–33744 (2013).

  • 22.

Mucke, L. & Selkoe, D. J. Neurotoxicity of amyloid β-protein: synaptic and network dysfunction. Cold Spring Harb. Perspect. Med. 2, a0063381 (2012).

  • 23.

Sebollela, A. et al. Amyloid-β oligomers induce differential gene expression in adult human brain slices. J. Biol. Chem. 287, 7436–7445 (2012).

  • 24.

Colaianni, G. et al. The myokine irisin increases cortical bone mass. Proc. Natl Acad. Sci. USA 112, 12157–12162 (2015).

  • 25.

Figueiredo, C. P. et al. Memantine rescues transient cognitive impairment caused by high-molecular-weight Aβ oligomers but not the persistent impairment induced by low-molecular-weight oligomers. J. Neurosci. 33, 9626–9634 (2013).

  • 26.

Lourenco, M. V. et al. TNF-α mediates PKR-dependent memory impairment and brain IRS-1 inhibition induced by Alzheimer’s β-amyloid oligomers in mice and monkeys. Cell Metab. 18, 831–843 (2013).

  • 27.

Jankowsky, J. L. et al. Co-expression of multiple transgenes in mouse CNS: a comparison of strategies. Biomol. Eng. 17, 157–165 (2001).

  • 28.

Cheng, A. et al. Involvement of PGC-1α in the formation and maintenance of neuronal dendritic spines. Nat. Commun. 3, 1250 (2012).

  • 29.

Holcomb, L. et al. Accelerated Alzheimer-type phenotype in transgenic mice carrying both mutant amyloid precursor protein and presenilin 1 transgenes. Nat. Med. 4, 97–100 (1998).

  • 30.

Ma, T. et al. Suppression of eIF2α kinases alleviates Alzheimer’s disease-related plasticity and memory deficits. Nat. Neurosci. 16, 1299–1305 (2013).

  • 31.

Yang, W. et al. Repression of the eIF2α kinase PERK alleviates mGluR-LTD impairments in a mouse model of Alzheimer’s disease. Neurobiol. Aging 41, 19–24 (2016).

  • 32.

Trinh, M. A. & Klann, E. Translational control by eIF2α kinases in long-lasting synaptic plasticity and long-term memory. Neurobiol. Learn. Mem. 105, 93–99 (2013).

  • 33.

Gong, B. et al. Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment. J. Clin. Invest. 114, 1624–1634 (2004).

  • 34.

Vitolo, O. V. et al. Amyloid β-peptide inhibition of the PKA/CREB pathway and long-term potentiation: reversibility by drugs that enhance cAMP signaling. Proc. Natl Acad. Sci. USA 99, 13217–13221 (2002).

  • 35.

Schaefer, N. et al. The malleable brain: plasticity of neural circuits and behavior: a review from students to students. J. Neurochem. 142, 790–811 (2017).

  • 36.

Katsnelson, A., De Strooper, B. & Zoghbi, H. Y. Neurodegeneration: from cellular concepts to clinical applications. Sci. Transl. Med. 8, 364ps318 (2016).

  • 37.

Selkoe, D. J. Alzheimer’s disease is a synaptic failure. Science 298, 789–791 (2002).

  • 38.

Lepeta, K. et al. Synaptopathies: synaptic dysfunction in neurological disorders: a review from students to students. J. Neurochem. 138, 785–805 (2016).

  • 39.

Zhang, Y. et al. Irisin stimulates browning of white adipocytes through mitogen-activated protein kinase p38 MAP kinase and ERK MAP kinase signaling. Diabetes 63, 514–525 (2014).

  • 40.

Timmons, J. A., Baar, K., Davidsen, P. K. & Atherton, P. J. Is irisin a human exercise gene? Nature 488, E9–E10 (2012).

  • 41.

Albrecht, E. et al. Irisin: a myth rather than an exercise-inducible myokine. Sci. Rep. 5, 8889 (2015).

  • 42.

Martin, K. C. & Kandel, E. R. Cell adhesion molecules, CREB, and the formation of new synaptic connections. Neuron 17, 567–570 (1996).

  • 43.

Suwabe, K. et al. Rapid stimulation of human dentate gyrus function with acute mild exercise. Proc. Natl Acad. Sci. USA 115, 10487–10492 (2018).

  • 44.

van Praag, H., Fleshner, M., Schwartz, M. W. & Mattson, M. P. Exercise, energy intake, glucose homeostasis, and the brain. J. Neurosci. 34, 15139–15149 (2014).

  • 45.

Neufer, P. D. et al. Understanding the cellular and molecular mechanisms of physical activity-induced health benefits. Cell Metab. 22, 4–11 (2015).

  • 46.

Baker, L. D. et al. Effects of aerobic exercise on mild cognitive impairment: a controlled trial. Arch. Neurol. 67, 71–79 (2010).

  • 47.

Buchman, A. S. et al. Total daily physical activity and the risk of AD and cognitive decline in older adults. Neurology 78, 1323–1329 (2012).

  • 48.

Okonkwo, O. C. et al. Physical activity attenuates age-related biomarker alterations in preclinical AD. Neurology 83, 1753–1760 (2014).

  • 49.

Müller, S. Relationship between physical activity, cognition, and Alzheimer pathology in autosomal dominant Alzheimer’s disease. Alzheimers Dement. 14, 1427–1437 (2018).

  • 50.

Mattson, M. P. Energy intake and exercise as determinants of brain health and vulnerability to injury and disease. Cell Metab. 16, 706–722 (2012).

  • 51.

Moon, H. Y. et al. Running-induced systemic cathepsin B secretion is associated with memory function. Cell Metab. 24, 332–340 (2016).

  • 52.

Sleiman, S. F. et al. Exercise promotes the expression of brain derived neurotrophic factor (BDNF) through the action of the ketone body β-hydroxybutyrate. eLife 5, e15092 (2016).

  • 53.

Smith, R. W., Wang, J., Bucking, C. P., Mothersill, C. E. & Seymour, C. B. Evidence for a protective response by the gill proteome of rainbow trout exposed to X-ray induced bystander signals. Proteomics 7, 4171–4180 (2007).

  • 54.

Mendes, N. D. et al. Free-floating adult human brain-derived slice cultures as a model to study the neuronal impact of Alzheimer’s disease-associated Aβ oligomers. J. Neurosci. Meth. 307, 203–209 (2018).

  • 55.

Drummond, C. et al. Deficits in narrative discourse elicited by visual stimuli are already present in patients with mild cognitive impairment. Front. Aging Neurosci. 7, 96 (2015).

  • 56.

Ledo, J. H. et al. Amyloid-β oligomers link depressive-like behavior and cognitive deficits in mice. Mol. Psychiatry 18, 1053–1054 (2013).

  • 57.

Ledo, J. H. et al. Cross talk between brain innate immunity and serotonin signaling underlies depressive-like behavior induced by Alzheimer’s amyloid-β oligomers in mice. J. Neurosci. 36, 12106–12116 (2016).

  • 58.

Trinchese, F. et al. Inhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease. J. Clin. Invest. 118, 2796–2807 (2008).

  • 59.

Alamed, J., Wilcock, D. M., Diamond, D. M., Gordon, M. N. & Morgan, D. Two-day radial-arm water maze learning and memory task; robust resolution of amyloid-related memory deficits in transgenic mice. Nat. Protoc. 1, 1671–1679 (2006).

  • 60.

Puzzo, D. et al. Phosphodiesterase 5 inhibition improves synaptic function, memory, and amyloid-β load in an Alzheimer’s disease mouse model. J. Neurosci. 29, 8075–8086 (2009).

  • 61.

Madeira, C. et al. d-serine levels in Alzheimer’s disease: implications for novel biomarker development. Transl. Psychiatry 5, e561 (2015).

  • 62.

Seixas Da Silva, G. S. et al. Amyloid-β oligomers transiently inhibits AMP-activated kinase and cause metabolic defects in hippocampal neurons. J. Biol. Chem. 292, 7395–7406 (2017).

  • 63.

Gong, B. et al. Ubiquitin hydrolase Uch-L1 rescues β-amyloid-induced decreases in synaptic function and contextual memory. Cell 126, 775–788 (2006).

  • 64.

De Felice, F. G. et al. Aβ oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine. J. Biol. Chem. 282, 11590–11601 (2007).

  • 65.

Lambert, M. P. et al. Monoclonal antibodies that target pathological assemblies of Aβ. J. Neurochem. 100, 23–35 (2007).

  • 66.

Abràmoff, M. D., Magalhães, P. J. & Ram, S. J. Image processing with ImageJ. Biophotonics Int. 11, 36–42 (2004).

  • 67.

Livak, K. J. & Schmittgen, T. D. Analysis of relative gene expression data using real-time quantitative PCR and the 2−ΔΔC T method. Methods 25, 402–408 (2001).

  • 68.

Brito-Moreira, J. et al. Interaction of amyloid-β (Aβ) oligomers with neurexin 2α and neuroligin 1 mediates synapse damage and memory loss in mice. J. Biol. Chem. 292, 7327–7337 (2017).

  • 69.

Schmidt, E. K., Clavarino, G., Ceppi, M. & Pierre, P. SUnSET, a nonradioactive method to monitor protein synthesis. Nat. Methods 6, 275–277 (2009).

  • 70.

Beckman, D. et al. Prion protein modulates monoaminergic systems and depressive-like behavior in mice. J. Biol. Chem. 290, 20488–20498 (2015).

sem título485858

sem título00sem título1aesem título444r

sem título00iii

sem título1xxxxxxxxx

 

10 Comments

  1. Increase Likes, Status Auto Liker, Autolike, Autolike International, Autoliker, ZFN Liker, Auto Liker, autoliker, Status Liker, Working Auto Liker, Auto Like, Photo Liker, auto like, Photo Auto Liker, auto liker, autolike, Autoliker

    Like

  2. Have you ever considered about including a little bit more than just
    your articles? I mean, what you say is important and everything.
    Nevertheless imagine if you added some great pictures or videos to give your
    posts more, “pop”! Your content is excellent but with pics and clips,
    this website could undeniably be one of the greatest in its field.
    Awesome blog!

    Like

  3. Hello! This is kind of off topic but I need some guidance from an established blog. Is it difficult to set up your own blog? I’m not very techincal but I can figure things out pretty fast. I’m thinking about making my own but I’m not sure where to begin. Do you have any points or suggestions? Thanks

    Like

  4. Viagra Suisse Prix Esotaabsor [url=https://ascialis.com/#]buy cheap generic cialis online[/url] FLOONSNURO Order Propecia Discount Hemsemboto cheapest cialis 20mg unfokeones cialis brand online

    Like

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s