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Loss of canonical Wnt signaling is involved in the pathogenesis of Alzheimer's disease

Neural Regeneration Research 2018年第10期13卷 1705-1710页

作者： cheril tapia-rojas Nibaldo C.Inestrosa Centro de Envejecimiento y Regeneración (CARE UC) Departamento de Biología Celular y MolecularFacultad de Ciencias BiológicasPontificia Universidad Católica de Chile Centre for Healthy Brain Ageing School of PsychiatryFaculty of MedicineUniversity of New South Wales Centro de Excelencia en Biomedicina de Magallanes (CEBIMA) Universidad de Magallanes

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.

关键词： Wnt signaling Wnt target genes Wnt/β-catenin Alzheimer disease amyloid-β tau phosphorylation memory loss synaptic dysfunction

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Phosphorylated tau as a toxic agent in synaptic mitochondria: implications in aging and Alzheimer’s disease

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Neural Regeneration Research 2022年第8期17卷 1645-1651页

作者： Angie K.Torres Bastián I.Rivera Catalina M.Polanco Claudia Jara cheril tapia-rojas Laboratory of Neurobiology of Aging Centro de Biología Celular y Biomedicina(CEBICEM)Facultad de Medicina y CienciaUniversidad San SebastiánSede Los LeonesSantiagoChile

During normal aging,there is a decline in all physiological functions in the *** of the most affected organs is the brain,where neurons lose their proper synaptic function leading to cognitive *** is one of the main risk factors for the development of neurodegenerative diseases,such as Alzheimer’s *** of the main responsible factors for synaptic dysfunction in aging and neurodegenerative diseases is the accumulation of abnormal proteins forming *** most studied brain aggregates are the senile plaques,formed by Aβpeptide;however,the aggregates formed by phosphorylated tau protein have gained relevance in the last years by their *** is reported that neurons undergo severe mitochondrial dysfunction with age,with a decrease in adenosine 5′-triphosphate production,loss of the mitochondrial membrane potential,redox imbalance,impaired mitophagy,and loss of calcium buffer ***,abnormal tau protein interacts with several mitochondrial proteins,suggesting that it could induce mitochondrial ***,whether tau-mediated mitochondrial dysfunction occurs indirectly or directly is still unknown.A recent study of our laboratory shows that phosphorylated tau at Ser396/404(known as PHF-1),an epitope commonly related to pathology,accumulates inside mitochondria during normal *** accumulation occurs preferentially in synaptic mitochondria,which suggests that it may contribute to the synaptic failure and cognitive impairment seen in aged ***,we review the main tau modifications promoting mitochondrial dysfunction,and the possible mechanism ***,we discuss the evidence that supports the possibility that phosphorylated tau accumulation in synaptic mitochondria promotes synaptic and cognitive impairment in ***,we show evidence and argue about the presence of phosphorylated tau PHF-1 inside mitochondria in Alzheimer’s disease,which could be considered as an early event

关键词： age pathology aging Alzheimer’s disease hippocampus memory mitochondria PHF-1 phosphorylated tau synaptic mitochondria tau

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儿童重症疾病时肾上腺的功能

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中华儿科杂志 2002年第9期40卷 535-535页

作者： Kusum Menon cheril Clarson 唐浩勋樊寻梅

目的　成人危重症及儿童感染性休克时肾上腺功能异常已得到阐述 ,未及时诊断与治疗者预后差。但有关其他儿童重症疾病时肾上腺的功能状态尚无报道。作者前瞻性地研究了危重患儿肾上腺功能异常的发生率。方法　以 13例小儿危重症评分≥ 1... 详细信息

目的　成人危重症及儿童感染性休克时肾上腺功能异常已得到阐述 ,未及时诊断与治疗者预后差。但有关其他儿童重症疾病时肾上腺的功能状态尚无报道。作者前瞻性地研究了危重患儿肾上腺功能异常的发生率。方法　以 13例小儿危重症评分≥ 10分和 (或 )血流动力学不稳定(应用血管活性药和 /或需要 2 0ml/kg液体扩容以保证血压稳定 )的患儿为研究对象。入选第 2天 7∶0 0～ 9∶0 0取血测皮质醇、促肾上腺皮质激素 (为基础值 ) ;静脉注射α 1,2 4 促肾上腺皮质激素 ,1h后再次取血检测上述指标。结果　皮质醇的基础值为 0 1～ 37 4 μg/dl [平均 (12 2± 9 6 ) μg/dl]。肾上腺功能不全的诊断标准为清晨皮质醇 <7μg/dl或注射ACTH后皮质醇 <18μg/dl。 13例中有 4例 (31% )肾上腺功能不全 ,其中皮质醇基础值 <7μg/dl的 3例的ACTH值均处于正常下限。发生与未发生肾上腺功能不全的患儿小儿危重评分 (14 7± 4 11、12 7± 2 6 5 ,P =0 37)与入院诊断无差异。结论　一些危重患儿在严重生理应激反应时不能产生足够的皮质醇 ,但对外源性ACTH反应良好。作者对危重症中下丘脑垂体肾上腺轴的作用进行了阐述。

关键词：儿童重症疾病肾上腺肾上腺功能异常

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