Article
Cell Biology
Yvette Akwa, Chiara Di Malta, Fatima Zallo, Elise Gondard, Adele Lunati, Lara Z. Diaz-de-Grenu, Angela Zampelli, Anne Boiret, Sara Santamaria, Maialen Martinez-Preciado, Katia Cortese, Jeffrey H. Kordower, Carlos Matute, Andres M. Lozano, Estibaliz Capetillo-Zarate, Thomas Vaccari, Carmine Settembre, Etienne E. Baulieu, Davide Tampellini
Summary: Synaptic stimulation promotes TFEB-mediated clearance of pathological MAPT/Tau, which provides neuroprotection. Deep brain stimulation activates TFEB and reduces MAPT/Tau levels in Parkinson disease patients, leading to neuroprotection.
Article
Chemistry, Multidisciplinary
Lingli Liu, Putu Andhita Dananjaya, Calvin Ching Ian Ang, Eng Kang Koh, Gerard Joseph Lim, Han Yin Poh, Mun Yin Chee, Calvin Xiu Xian Lee, Wen Siang Lew
Summary: A three-terminal memristor based on oxygen ion migration is developed to function as both a synapse and a neuron. It exhibits short-term plasticity and learning capability, and can emulate the leaky-integrate-and-fire neuronal model by leveraging short-term dynamics. The proposed 3TM offers more process compatibility for integrating synaptic and neuronal components in the hardware implementation of a spiking neural network.
Article
Immunology
Xiao-ying Sun, Ling-jie Li, Quan-Xiu Dong, Jie Zhu, Ya-ru Huang, Sheng-jie Hou, Xiao-lin Yu, Rui-tian Liu
Summary: The study demonstrated that rutin could inhibit tau aggregation and tau oligomer-induced cytotoxicity, reduce the production of proinflammatory cytokines, protect neuronal morphology from toxic tau oligomers, and promote microglial uptake of extracellular tau oligomers. In a Tau-P301S mouse model, rutin also reduced pathological tau levels, regulated tau hyperphosphorylation, suppressed gliosis and neuroinflammation, prevented microglial synapse engulfment, and rescued synapse loss, resulting in a significant improvement of cognition. These findings suggest that rutin is a promising drug candidate for Alzheimer's disease treatment by targeting both tau and amyloid beta pathology.
JOURNAL OF NEUROINFLAMMATION
(2021)
Article
Mathematics
Osman Taylan, Mona Abusurrah, Ehsan Eftekhari-Zadeh, Ehsan Nazemi, Farheen Bano, Ali Roshani
Summary: This paper investigates the regulatory role of astrocyte cells in neuronal activity and presents a model to describe their interactions. Simulation results demonstrate that by adjusting the coupling coefficients of astrocytes, the spiking frequency of neurons can be reduced and the activity of neuronal cells can be modulated.
Article
Biochemistry & Molecular Biology
Edward Chau, Hyunjoo Kim, Jineun Shin, Alberto Martinez, Jin Ryoun Kim
Summary: The study found that AM17 can not only inhibit the aggregation of alpha S monomers, but also disaggregate alpha S oligomers and fibrils, independent of copper ions. Resveratrol also showed similar inhibitory effects on alpha S aggregation only in the presence of copper ions.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2021)
Article
Mathematics
Sergey V. Stasenko, Alexey N. Mikhaylov, Victor B. Kazantsev
Summary: This study investigates an unstructured neuron network model consisting of excitatory and inhibitory neurons, and explores the application of memristors with spike timing-dependent plasticity (STDP) characteristics in the network. The findings reveal that memristor-based STDP for inhibitory connections can suppress bursting dynamics and induce random spiking mode in the network. These results contribute to the advancement of invasive neurointerfaces and the understanding and control of epileptiform activity.
Article
Medicine, Research & Experimental
Hua-Li Wan, Xiao-Yue Hong, Zai-Hua Zhao, Ting Li, Bing-Ge Zhang, Qian Liu, Qun Wang, Shi Zhao, Jian-Zhi Wang, Xue-Feng Shen, Gong-Ping Liu
Summary: The study revealed that hTau accumulation inactivated STAT3 by acetylating STAT1, leading to suppression of NMDARs expression, affecting synaptic plasticity and causing memory deficits.
Article
Biochemistry & Molecular Biology
Mueed Ur Rahman, Ashfaq Ur Rehman, Taaha Arshad, Hai-Feng Chen
Summary: The study reveals the disaggregation mechanism of Amyloid using molecular tweezer CLR01, showing that CLR01 can effectively disaggregate amyloid by interacting with Lysine and stretching out the N-terminal chain. Furthermore, CLR01 remodels the pentamer Prion into a compact structure, which may resist further oligomerization.
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
(2021)
Correction
Clinical Neurology
Woo Shik Shin, Jing Di, Qin Cao, Binsen Li, Paul M. Seidler, Kevin A. Murray, Gal Bitan, Lin Jiang
Summary: The paper has been amended and the updated version can be accessed through the original article.
ALZHEIMERS RESEARCH & THERAPY
(2021)
Article
Biochemistry & Molecular Biology
M. Paul Murphy, Valeria A. Buzinova, Carrie E. Johnson
Summary: Progress has been made in the treatment of Alzheimer's disease through the development of anti-A beta therapeutics, which have shown modest efficacy in slowing the progression of the disease. However, the puzzling issue remains as to why completely removing A beta does not fully stop the disease.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
(2024)
Article
Chemistry, Multidisciplinary
Oxana V. Galzitskaya, Olga M. Selivanova, Elena Y. Gorbunova, Leila G. Mustaeva, Viacheslav N. Azev, Alexey K. Surin
Summary: Under certain conditions, proteins and peptides can self-assemble into various supramolecular structures with potential pathological or functional implications. Fibrils, films, and amyloid gels are promising objects for nanobiotechnology research. Understanding the mechanism of structure formation and its influencing factors is crucial for developing nanobiomaterials with desired properties.
Article
Multidisciplinary Sciences
Yunpeng Sun, Houfang Long, Wencheng Xia, Kun Wang, Xia Zhang, Bo Sun, Qin Cao, Yaoyang Zhang, Bin Dai, Dan Li, Cong Liu
Summary: The study demonstrates that the G51D mutation induces a distinct fibril strain of alpha-syn in vitro, with the corresponding structure determined by cryo-EM.
NATURE COMMUNICATIONS
(2021)
Article
Biochemistry & Molecular Biology
Pol Andres-Benito, Africa Flores, Sara Busquet-Areny, Margarita Carmona, Karina Ausin, Paz Cartas-Cejudo, Mercedes Lachen-Montes, Jose Antonio Del Rio, Joaquin Fernandez-Irigoyen, Enrique Santamaria, Isidro Ferrer
Summary: Transcriptomics and phosphoproteomics analyses revealed altered gene expression and phosphorylation levels in the cerebral cortex of tau knockout mice. Tau knockout mice exhibited reduced anxiety-like behavior and fear expression, while recognition memory remained unchanged. The altered gene expression affected synaptic structures, neuron cytoskeleton, transport, and extracellular matrix components, while the deregulated phosphorylation levels impacted cytoskeletal and membrane proteins, DNA and RNA metabolism, and various signaling pathways.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Cell Biology
Laura C. Graham, Rachel A. Kline, Douglas J. Lamont, Thomas H. Gillingwater, Neil A. Mabbott, Paul A. Skehel, Thomas M. Wishart
Summary: Proteomic analysis of synaptic and non-synaptic mitochondria in mice revealed unique protein expression profiles in aged synaptic mitochondria. Recapitulation of aged synaptic mitochondrial protein expression in the Drosophila neuromuscular junction disrupted synaptic architecture, indicating that temporal regulation of the mitochondrial proteome may directly modulate synaptic stability.
Review
Neurosciences
Oriol Busquets, Antoni Parcerisas, Ester Verdaguer, Miren Ettcheto, Antoni Camins, Carlos Beas-Zarate, Ruben Dario Castro-Torres, Carme Auladell
Summary: This review discusses the involvement of c-Jun N-terminal Kinases (JNKs) in early alterations of Alzheimer's disease (AD), including synaptic loss and dysregulation of neuronal transport. The interactions between JNKs and these processes contribute to cognitive decline in AD, with disruptions in cellular processes such as glutamatergic, GABA, and cholinergic synapses. Furthermore, the review highlights the role of the JNK-JIP complex in controlling neuronal transport and the impact of amyloid-beta aggregates and hyperphosphorylated tau on this process.
JOURNAL OF ALZHEIMERS DISEASE
(2021)