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| 1 | Loss of canonical Wnt signaling is involved in the pathogenesis of Alzheimer's disease显示文摘Alzheimer's disease(AD) is the most common form of dementia in the older population, however, the precise cause of the disease is unknown. The neuropathology is characterized by the presence of aggregates formed by amyloid-β(Aβ) peptide and phosphorylated tau; which is accompanied by progressive impairment of memory. Diverse signaling pathways are linked to AD, and among these the Wnt signaling pathway is becoming increasingly relevant, since it plays essential roles in the adult brain. Initially, Wnt signaling activation was proposed as a neuroprotective mechanism against Aβ toxicity. Later, it was reported that it participates in tau phosphorylation and processes of learning and memory. Interestingly, in the last years we demonstrated that Wnt signaling is fundamental in amyloid precursor protein(APP) processing and that Wnt dysfunction results in Aβ production and aggregation in vitro. Recent in vivo studies reported that loss of canonical Wnt signaling exacerbates amyloid deposition in a transgenic(Tg) mouse model of AD. Finally, we showed that inhibition of Wnt signaling in a Tg mouse previously at the appearance of AD signs, resulted in memory loss, tau phosphorylation and Aβ formation and aggregation; indicating that Wnt dysfunction accelerated the onset of AD. More importantly, Wnt signaling loss promoted cognitive impairment, tau phosphorylation and Aβ1–42 production in the hippocampus of wild-type(WT) mice, contributing to the development of an Alzheimer's-like neurophatology. Therefore, in this review we highlight the importance of Wnt/β-catenin signaling dysfunction in the onset of AD and propose that the loss of canonical Wnt signaling is a triggering factor of AD. | Cheril Tapia-Rojas Nibaldo C.Inestrosa | 2018 | Neural Regeneration Research2018，13，10： | 21 |
| 2 | Wnt signaling in the nervous system and in Alzheimer's disease显示文摘Wnts 包括出现了是包括 organogenesis,中脑发展以及干细胞增长调整几 aspectsof 开发的发信号的串联的部分的蛋白质的一个大家庭。在在成年大脑的 neuronal 电路并且也的发展的 Wnt 发信号小径 playsdifferent 角色,在它调整 synaptic transmissionand 的地方粘性。它也包括癌症和 neurodegenerative 疾病在各种各样的疾病被含有,在基本生物过程的 reflectingits 关联。这评论与 Alzheimer 的疾病(广告) 的一个焦点在成熟 nervoussystem 关于 Wnts 功能总结进步。我们讨论正规的 modulating 和不在经典中的 Wnt signalingas 的前景为 neuroprotection 的策略。这将包括 Wnts 的潜力到:是的(i) 行为在学习和记忆的 hippocampalsynapses 和影响的有势力管理者;(ii ) 调整成年神经发生;并且(iii ) 最后控制广告致病。 | Nibaldo C. Inestrosa Lorena Varela-Nallar | 2014 | Journal of Molecular Cell Biology2014，8，1： | 14 |
| 3 | Acetylcholinesterase accderates assembly of amyloid-β-peptides into Azheimer' s fibrils : Possible role of the peribheral site of the enzyme显示文摘 | Nibaldo C Inestrosa Alejandra A | 1996 | Neuron1996，16，： | 1 |
| 4 | Circadian stress tolerance in adult Caenorhabditis elegans显示文摘 | Sergio H. Simonetta Andrés Romanowski Alicia N. Minniti Nibaldo C. Inestrosa Diego A. Golombek | 2008 | Journal of Comparative Physiology A2008，，9： | 1 |
| 5 | Diterpenes and the crosstalk with the arachidonic acid pathways, relevance in neurodegeneration显示文摘Dementia has emerged as one of the main threats to human health in the modern civilization. Increased aging of world population and unhealthy lifestyle habits have been identified as critical factors able to facilitate dementia establishment. In this context, according to the Alzheimer’s Research International, Alzheimer’s disease (AD) constitutes the primary cause of dementia worldwide and its numbers are expected to grow during the following years. Clinically, AD is characterized by the progressive decline in the cognitive performance as well as by an altered social behavior. Initially affecting the short-term memory, the long-term memory becomes compromised as the pathology progresses. | Juan M. Zolezzi Nibaldo C. Inestrosa | 2019 | Neural Regeneration Research2019，14，10： | 1 |
| 6 | Emerging roles of Wnts in the adult nervous system显示文摘 | Nibaldo C Arenas IE | | 0，，： | 1 |
| 7 | Wnt signaling in neuroprotection and stem cell differentiation显示文摘 | Enrique M. Toledo Marcela Colombres Nibaldo C. Inestrosa | 2008 | Progress in Neurobiology2008，，3： | 1 |
| 8 | Emerging roles of Wnts in the adult nervous system显示文摘 | Nibaldo C Inestrosa E Arenas | 2010 | Nat Rev Neurosci2010，11，2： | 1 |
| 9 | Wnt Signaling:Role in Alzheimer Disease and Schizophrenia显示文摘 | Nibaldo C Inestrosa Carla Montecinos-Oliva Marco Fuenzalida | 2012 | J Neuroimmune Pharmacol2012，7，4： | 1 |
| 10 | Peroxisome Proliferator-activated Receptors and Alzheimer’s Disease: Hitting the Blood–Brain Barrier显示文摘 | Juan M. Zolezzi Nibaldo C. Inestrosa | 2013 | Molecular Neurobiology2013，，3： | 1 |
| 11 | Structure and function of amyloid in Alzheimer’s disease显示文摘 | Carlos Morgan Marcela Colombres Marco Tulio Nu?ez Nibaldo C. Inestrosa | 2004 | Progress in Neurobiology2004，，6： | 1 |
| 12 | Wnt Signaling: Role in Alzheimer Disease and Schizophrenia显示文摘 | Nibaldo C. Inestrosa Carla Montecinos-Oliva Marco Fuenzalida | 2012 | Journal of Neuroimmune Pharmacology2012，，4： | 1 |
| 13 | Tetrahydrohyperforin:a neuroprotective modified natural compound against Alzheimer's disease显示文摘According to the World Health Organization(WHO),a total of 35.6 million cases of dementia were estimated in 2010,with close to 7.7 million new cases each year.In 2008,WHO declared dementia a priority condition.90%of all dementia cases are considered to be Alzheimer’s disease(AD).Therefore,great effort was made to understand the etiology of | Carla Montecinos-Oliva Andreas Schüller Nibaldo C.Inestrosa | 2015 | Neural Regeneration Research2015，10，4： | 0 |
| 14 | Tetrahydrohyperforin(IDN5706) targets the endoplasmic reticulum for autophagy activation: potential mechanism for Alzheimer's disease therapy显示文摘Alzheimer’s disease(AD)is the most common form of dementia worldwide among the older population.To date,there is no therapy to stop the destruction of brain cells and all the available treatments only compensate for the loss of synaptic transmission,thus resulting in marginal benefits to patients. | alexis gonzález viviana a.cavieres nibaldo c.inestrosa patricia v.burgos | 2016 | Neural Regeneration Research2016，11，2： | 0 |
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