Article
Cell Biology
Abubakar Wani, Sweilem B. Al Rihani, Ankita Sharma, Brenna Weadick, Rajgopal Govindarajan, Sameer U. Khan, Parduman R. Sharma, Ashish Dogra, Utpal Nandi, Chilakala N. Reddy, Sonali S. Bharate, Gurdarshan Singh, Sandip B. Bharate, Ram A. Vishwakarma, Amal Kaddoumi, Ajay Kumar
Summary: This study found that crocetin can induce autophagy in Alzheimer's disease, helping to clear Aβ and improve memory function.
Article
Cell Biology
Xiaoyan Xu, Yaqin Sun, Xufeng Cen, Bing Shan, Qingwei Zhao, Tingxue Xie, Zhe Wang, Tingjun Hou, Yu Xue, Mengmeng Zhang, Di Peng, Qiming Sun, Cong Yi, Ayaz Najafov, Hongguang Xia
Summary: The study reveals that Metformin can induce CMA through activating the TAK1-IKKα/β signaling pathway to improve the pathogenesis of neurodegenerative diseases. Additionally, Metformin can reduce amyloid-beta plaques in the brain and reverse the molecular and behavioral phenotypes of Alzheimer's disease.
Article
Cell Biology
Jia-Jun Wu, Haitao Yu, Shu-Guang Bi, Zhong-Xuan Wang, Juan Gong, Yu-Ming Mao, Fang-Zhou Wang, Yu-Qi Zhang, Yun-Juan Nie, Gao-Shang Chai
Summary: Growing evidence suggests that aerobic exercise can reverse autophagy-lysosomal deficits and attenuate amyloid-beta pathology in Alzheimer's disease. The molecular mechanism involves the activation of ADRB2/beta 2-adrenergic receptor and upregulation of AMPK-MTOR signaling pathway. AE can also enhance V-ATPase function by upregulating VMA21 levels. The inhibition of ADRB2 blocks the beneficial effects of AE on A beta pathology and cognitive deficits.
Review
Cell Biology
Yi-Ting Wang, Jia-Hong Lu
Summary: Chaperone-mediated autophagy (CMA) is a protein degradation mechanism associated with neurodegenerative diseases (NDs). Modulating CMA has been shown to promote the degradation of ND-associated proteins and alleviate ND phenotypes, making it a potential therapeutic strategy for ND.
Article
Medicine, Research & Experimental
Yuening Luo, Siqi Zhou, Haruna Haeiwa, Reiko Takeda, Kazuma Okazaki, Marie Sekita, Takuya Yamamoto, Mikio Yamano, Kazuichi Sakamoto
Summary: The study found that amber extract reduces neuronal cell apoptosis induced by amyloid beta by regulating oxidative stress pathways and protein expression levels, suggesting it may be a potential treatment for Alzheimer's disease.
BIOMEDICINE & PHARMACOTHERAPY
(2021)
Article
Oncology
Claudia Matlakala Ntsapi, Ben Loos
Summary: Alzheimer's disease is a devastating neurodegenerative condition with significant socio-economic impact, exacerbated by rapid population aging. Accumulation of the Aβ peptide, driven by the amyloid precursor protein processing, plays a key role in synaptic dysfunction and neuronal cell loss associated with AD pathogenesis. Modulation of autophagy for enhanced Aβ clearance has shown promising therapeutic potential in neuronal protection.
EXPERIMENTAL CELL RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Rui Xiong, Dan Shao, Sandra Do, William K. Chan
Summary: This study investigated the degradation mechanism of the aryl hydrocarbon receptor (AHR) in the lung using human lung epithelial A549 cells. The findings suggest that chaperone-mediated autophagy (CMA) can decrease AHR protein levels, thereby suppressing the expression of AHR target genes, and that mutations in AHR's CMA motif result in resistance to CMA.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Geriatrics & Gerontology
Minjie Wu, Noah Schweitzer, Bistra E. Iordanova, Edythe Halligan-Eddy, Dana L. Tudorascu, Chester A. Mathis, Brian J. Lopresti, M. Ilyas Kamboh, Ann D. Cohen, Beth E. Snitz, William E. Klunk, Howard J. Aizenstein
Summary: This study explored the interactive effects of small vessel disease (SVD) and amyloid-beta (Aβ) pathology on hippocampal functional connectivity and volume in cognitively normal older adults. The results showed that in older adults with white matter hyperintensities (WMH+), higher Aβ burden was associated with increased hippocampal local connectivity and lower gray matter density in the medial temporal lobe (MTL). In older adults without WMH, higher Aβ burden was associated with increased hippocampal distal connectivity and no changes in MTL gray matter density. These findings provide support for a hippocampal excitotoxicity model linking SVD to neurodegeneration and the progression to Alzheimer's disease (AD).
AMERICAN JOURNAL OF GERIATRIC PSYCHIATRY
(2023)
Article
Neurosciences
Meiting Li, Nan Cai, Liang Gu, Lijun Yao, Decheng Bi, Weishan Fang, Zhijian Lin, Yan Wu, Hong Xu, Hui Li, Zhangli Hu, Xu Xu
Summary: Genipin shows promising effects on inhibiting Tau aggregation and Aβ generation through multiple molecular mechanisms, making it a potential therapeutic agent or nutraceutical for Alzheimer's disease.
MOLECULAR NEUROBIOLOGY
(2021)
Article
Cell Biology
Diana M. Bessa de Sousa, Ariane Benedetti, Barbara Altendorfer, Heike Mrowetz, Michael S. Unger, Katharina Schallmoser, Ludwig Aigner, Kathrin Maria Kniewallner
Summary: In Alzheimer's disease, dysfunctional platelets may contribute to amyloid beta deposition. Platelet depletion in APP-PS1 transgenic mice led to an increase in amyloid plaque size distribution and neuritic dystrophy in the hippocampus of female mice. It was found that platelet-depleted females had lower amounts of amyloid beta cargo and increased overlap between astrocytic processes and amyloid plaques. These findings suggest that platelets might limit plaque growth and reduce plaque-related neuritic dystrophy at advanced stages of amyloid plaque pathology in APP-PS1 female mice.
Article
Neurosciences
Yunzhu Yang, Jiafa Zhang, Canhong Yang, Bo Dong, Yanhong Fu, Yuanyuan Wang, Ming Gong, Tao Liu, Pingming Qiu, Weibing Xie, Tianming Lu
Summary: The study showed that sulforaphane played a protective role on neurons by inhibiting autophagy initiation, autophagic lysosomal membrane permeability, and NLRP3/caspase-1 inflammasomes activation in Aβ-activated microglia. It also inhibited M1 phenotype polarization. These findings provide new insights into the potential role of sulforaphane in AD therapy.
Review
Cell Biology
Haruo Kanno, Kyoichi Handa, Taishi Murakami, Toshimi Aizawa, Hiroshi Ozawa
Summary: Autophagy is an important cellular function involved in the degradation of proteins and organelles. Chaperone-mediated autophagy (CMA) specifically degrades proteins and plays a crucial role in maintaining cellular proteostasis. Dysfunction of CMA is associated with the accumulation of toxic protein aggregates in the central nervous system (CNS) and contributes to the pathogenesis of neurodegenerative diseases. Recent studies have shown that CMA activity is upregulated in damaged neural tissue following acute neurological insults, suggesting its role in neuroprotection. Enhancing CMA pathway may have therapeutic potential for both neurodegenerative diseases and acute neurological injuries.
Review
Cell Biology
Simon Schnebert, Maxime Goguet, Emilio J. Velez, Alexandra Depince, Florian Beaumatin, Amaury Herpin, Iban Seiliez
Summary: In this paper, an in-depth analysis of the evolutionary history of the main components of chaperone-mediated autophagy (CMA) and endosomal microautophagy (eMI) is presented, along with a discussion on how the observed differences between species may contribute to our understanding of these two functions and their interplays.
Review
Immunology
Chieko Matsui, Putu Yuliandari, Lin Deng, Takayuki Abe, Ikuo Shoji
Summary: Lysosomes degrade proteins through autophagy, with CMA being a selective degradation pathway using the KFERQ motif. Hepatitis C virus NS5A interacts with HSC70 and HNF-1α to promote CMA-induced lysosomal degradation, contributing to HCV pathogenesis. Further study of CMA-targeting proteins interacting with HCV NS5A may provide insights into HCV-induced pathogenesis.
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
(2021)
Article
Neurosciences
Zhongkang Zhu, Yuxi Liu, Xinyun Li, Lin Zhang, Huihui Liu, Yong Cui, Yanjie Wang, Danyu Zhao
Summary: High expression of GPNMB in the brain of Alzheimer's disease patients may facilitate Aβ clearance and improve AD-like behaviors through enhancing autophagy while suppressing the mTOR signal, providing novel strategies for the prevention and treatment of AD.
NEUROSCIENCE LETTERS
(2022)