Comparative the efficacy and safety of Gosuranemab, Semorinemab, Tilavonemab, and Zagotenemab in patients with Alzheimer’s disease: a systematic review and network meta-analysis of... by Wenting Cai, Wenting Cai, Hui Zhang, Hui Zhang, Yan Wu, Yan Wu, Yao Yao, Jinping Zhang

“…ObjectiveThe aim of this study was to compare the efficacy and safety of anti-tau protein monoclonal antibodies for Alzheimer’s disease (AD). Tau protein aggregation, a key pathological feature of AD, is closely associated with neurodegeneration and cognitive decline. …”
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Linking Neuroinflammation and Neurodegeneration in Parkinson’s Disease by Géraldine Gelders, Veerle Baekelandt, Anke Van der Perren

“…Nevertheless, several questions remain unanswered regarding the role of misfolded protein aggregates and the cause of neuronal cell death. …”
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Alternative Macroautophagic Pathways by Katrin Juenemann, Eric A. Reits

“…Macroautophagy is a bulk degradation process that mediates the clearance of long-lived proteins, aggregates, or even whole organelles. This process includes the formation of autophagosomes, double-membrane structures responsible for delivering cargo to lysosomes for degradation. …”
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Selective Autophagy in Drosophila by Ioannis P. Nezis

“…Autophagy functions as a cellular response in nutrient starvation, but it is also associated with the removal of protein aggregates and damaged organelles and therefore plays an important role in the quality control of proteins and organelles. …”
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Autophagy: More Than a Nonselective Pathway by Fulvio Reggiori, Masaaki Komatsu, Kim Finley, Anne Simonsen

“…Autophagy is a catabolic pathway conserved among eukaryotes that allows cells to rapidly eliminate large unwanted structures such as aberrant protein aggregates, superfluous or damaged organelles, and invading pathogens. …”
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Enhancing sleep quality in synucleinopathies through physical exercise by Jacopo Canonichesi, Laura Bellingacci, Francesco Rivelli, Alessandro Tozzi

“…Synucleinopathies are neurodegenerative disorders characterized by abnormal build-up of α-synuclein protein aggregates in the brain. This accumulation in different brain regions leads to a spectrum of clinical manifestations, including hypokinesia, cognitive impairment, psychiatric symptoms, and neurovegetative disturbances. …”
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Autophagy-associated signal pathways of functional foods for chronic diseases by Jinfeng Xie, Jiling Liang, Ning Chen

“…Once the cells are in the stress environment, the induced autophagy will accelerate the clearance of cellular damaged or toxic protein aggregates or dysfunctional cellular organelles to maintain homeostasis in cells. …”
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Therapeutic Actions of the Thiazolidinediones in Alzheimer’s Disease by María José Pérez, Rodrigo A. Quintanilla

“…Alzheimer’s disease (AD) is a multifactorial metabolic brain disorder characterized by protein aggregates, synaptic failure, and cognitive impairment. …”
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Maturation and detoxification of synphilin-1 inclusion bodies regulated by sphingolipids by Xiuling Cao, Xiang Wu, Lei Zhao, Ju Zheng, Xuejiao Jin, Xinxin Hao, Joris Winderickx, Shenkui Liu, Lihua Chen, Beidong Liu

“…Our findings identify a conserved cellular component essential for IB maturation and suggest a mechanism by which cells may detoxify the pathogenic protein aggregates through forming mitochondrion-associated IBs.…”
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Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival by Luke R. K. Hughson, Vincent I. Poon, Jaeline E. Spowart, Julian J. Lum

“…Accumulating evidence indicates that therapies designed to trigger apoptosis in tumor cells cause mitochondrial depolarization, nuclear damage, and the accumulation of misfolded protein aggregates, resulting in the activation of selective forms of autophagy. …”
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Aspirin inhibits proteasomal degradation and promotes α-synuclein aggregate clearance through K63 ubiquitination by Jing Gao, Yang Liu, Chenfang Si, Rui Guo, Shouqiao Hou, Xiaosong Liu, Houfang Long, Di Liu, Daichao Xu, Zai-Rong Zhang, Cong Liu, Bing Shan, Christoph W. Turck, Kaiwen He, Yaoyang Zhang

“…Accordingly, using the major pathological protein of Parkinson’s disease (PD), α-synuclein (α-syn), as an example of protein aggregates, we find that aspirin is able to reduce α-syn in cultured cells, neurons, and PD model mice with rescued locomotor ability. …”
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STRUCTURAL AND DYNAMIC PROPERTIES OF MUTANTS OF THE SOD1 PROTEIN ASSOCIATED WITH AMYOTROPHIC LATERAL SCLEROSIS by N. A. Alemasov, N. V. Ivanisenko, V. A. Ivanisenko

“…One of the causes of motor neuron degeneration and death is the formation of intracellular protein aggregates formed by a mutant SOD1 protein. Recently, it has been shown that the survival time of ALS patients with specific mutation in SOD1 gene inversely correlates with thermodynamic stability of the SOD1 mutant protein. …”
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Oxidative Stress, DNA Damage, and c-Abl Signaling: At the Crossroad in Neurodegenerative Diseases? by Stefania Gonfloni, Emiliano Maiani, Claudia Di Bartolomeo, Marc Diederich, Gianni Cesareni

“…This suggests that aberrant nonspecific posttranslational modifications induced by c-Abl may contribute to fuel the recurrent phenotypes/features linked to neurodegenerative disorders, such as an impaired mitochondrial function, oxidative stress, and accumulation of protein aggregates. Herein, we review some reports on c-Abl function in neuronal cells and we propose that modulation of different aspects of c-Abl signaling may contribute to mediate the molecular events at the interface between stress signaling, metabolic regulation, and DNA damage. …”
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Amyloid Imaging in Aging and Dementia: Testing the Amyloid Hypothesis In Vivo by G. D. Rabinovici, W. J. Jagust

“…Amyloid imaging represents a major advance in neuroscience, enabling the detection and quantification of pathologic protein aggregations in the brain. In this review we survey current amyloid imaging techniques, focusing on positron emission tomography (PET) with ^{11}carbon-labelled Pittsburgh Compound-B (11C-PIB), the most extensively studied and best validated tracer. …”
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Advances in synaptic PET imaging and intervention with synapse-targeted small-molecular drugs for dementia diagnosis and therapy by Xiuhong Lu, Bin Ji, Gang Huang, Hong Ding

“…Repeated failure of dementia clinical trials with therapeutic drugs targeting abnormal protein aggregates has caused researchers to shift their focus to synaptic functions and increased the importance of clinically available imaging for synaptic density and the development of synapse-targeted intervention. …”
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Engineering a membrane protein chaperone to ameliorate the proteotoxicity of mutant huntingtin by Jeonghyun Oh, Christy Catherine, Eun Seon Kim, Kwang Wook Min, Hae Chan Jeong, Hyojin Kim, Mijin Kim, Seung Hae Ahn, Nataliia Lukianenko, Min Gu Jo, Hyeon Seok Bak, Sungsu Lim, Yun Kyung Kim, Ho Min Kim, Sung Bae Lee, Hyunju Cho

“…Abstract Toxic protein aggregates are associated with various neurodegenerative diseases, including Huntington’s disease (HD). …”
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MAP1B Interaction with the FW Domain of the Autophagic Receptor Nbr1 Facilitates Its Association to the Microtubule Network by Katie Marchbank, Sarah Waters, Roland G. Roberts, Ellen Solomon, Caroline A. Whitehouse

“…Selective autophagy is a process whereby specific targeted cargo proteins, aggregates, or organelles are sequestered into double-membrane-bound phagophores before fusion with the lysosome for protein degradation. …”
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Dysregulation of the Autophagy-Endolysosomal System in Amyotrophic Lateral Sclerosis and Related Motor Neuron Diseases by Asako Otomo, Lei Pan, Shinji Hadano

“…Although it remains to be determined whether disease-associated protein aggregates have a toxic or protective role in the pathogenesis, the formation of them results from the imbalance between generation and degradation of misfolded proteins within neuronal cells. …”
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Conformational and Functional Properties of Soybean Proteins Produced by Extrusion-Hydrolysis Approach by Wenjun Ma, Baokun Qi, Rokayya Sami, Lianzhou Jiang, Yang Li, Hui Wang

“…The increase of molecular weights could be attributed to the formation of protein aggregates during extrusion. Extrusion and enzymatic hydrolysis led to a sharp increase in the number of disulfide bonds with a decrease of the sulphydryl group. …”
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Oligonucleotide-Based Therapy for FTD/ALS Caused by the C9orf72 Repeat Expansion: A Perspective by Stephanie A. Fernandes, Andrew G. L. Douglas, Miguel A. Varela, Matthew J. A. Wood, Yoshitsugu Aoki

“…Two basic mechanisms have been proposed as being potentially responsible for c9FTD/ALS: loss-of-function of the protein encoded by this gene (associated with aberrant DNA methylation) and gain of function through the formation of RNA foci or protein aggregates. These diseases currently lack any cure or effective treatment. …”
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