Review
Biochemistry & Molecular Biology
Sarah Jane Annesley, Paul Robert Fisher
Summary: The study of mitochondrial function in neurological disorders is challenging due to the inaccessibility of brain tissue, but the use of lymphoblastoid cell lines (LCLs) is an effective approach. These cell models can help understand mitochondrial defects, signaling pathways, and biomarkers in neurological disorders, and are valuable for the development of diagnostic tests and identification of drug targets.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Neurosciences
Oscar Ramos-Campoy, Albert Llado, Beatriz Bosch, Mireia Ferrer, Agnes Perez-Millan, Miguel Vergara, Laura Molina-Porcel, Laura Fort-Aznar, Ricardo Gonzalo, Fermin Moreno-Izco, Guadalupe Fernandez-Villullas, Mircea Balasa, Raquel Sanchez-Valle, Anna Antonell
Summary: This study investigates gene expression profiles in different forms of Alzheimer's disease (AD) and frontotemporal dementia (FTD) using brain tissue and lymphoblastoid cell lines (LCLs). The findings reveal common altered pathways such as inflammation, glial cell differentiation, synaptic signaling, metabolism, and mitochondrial dysfunction in these diseases. The use of LCLs provides a potential method for studying early immune system and inflammation as well as neural features in neurodegenerative dementias.
MOLECULAR NEUROBIOLOGY
(2022)
Article
Multidisciplinary Sciences
Chunyu Liu, Jessica L. Fetterman, Xianbang Sun, Kaiyu Yan, Poching Liu, Yan Luo, Jun Ding, Jun Zhu, Daniel Levy
Summary: This study compared mtDNA sequence variants between LCL and whole blood samples. The results showed that most homoplasmic variants were present in both LCL and blood samples, while most heteroplasmic variants were unique to either LCL or blood samples. LCL samples had a higher number of heteroplasmic variants compared to whole blood samples, but a similar number of homoplasmic variants. Additionally, LCL samples tended to have lower levels of heteroplasmy.
SCIENTIFIC REPORTS
(2022)
Article
Biology
Nunzia Mollo, Matteo Esposito, Miriam Aurilia, Roberta Scognamiglio, Rossella Accarino, Ferdinando Bonfiglio, Rita Cicatiello, Maria Charalambous, Claudio Procaccini, Teresa Micillo, Rita Genesio, Gaetano Cali, Agnese Secondo, Simona Paladino, Giuseppe Matarese, Gabriella De Vita, Anna Conti, Lucio Nitsch, Antonella Izzo
Summary: Down syndrome, caused by an extra copy of chromosome 21, is associated with mental retardation and defects in neuronal development potentially due to mitochondrial dysfunction. Stem cells derived from individuals with Down syndrome showed a propensity towards developing as glial cells and exhibited early mitochondrial defects. This model can be used to further study the impact of mitochondrial dysfunction on neuronal development.
Article
Geriatrics & Gerontology
Chen Chen, Yao Chen, Zhong-Hao Zhang, Shi-Zheng Jia, Yu-Bin Chen, Shao-Ling Huang, Xin-Wen Xu, Guo-Li Song
Summary: Selenomethionine (Se-Met) improves mitochondrial function in Alzheimer's disease (AD) models by upregulating mitochondrial selenoprotein, promoting mitochondrial fusion or division, restoring mitochondrial membrane potential, enhancing mitochondrial energy metabolism, inhibiting intracellular ROS generation, and reducing apoptosis.
FRONTIERS IN AGING NEUROSCIENCE
(2021)
Review
Pharmacology & Pharmacy
Arunkumar Subramanian, T. Tamilanban, Abdulrhman Alsayari, Gobinath Ramachawolran, Ling Shing Wong, Mahendran Sekar, Siew Hua Gan, Vetriselvan Subramaniyan, Suresh V. V. Chinni, Nur Najihah Izzati Mat Rani, Nagaraja Suryadevara, Shadma Wahab
Summary: The primary and significant weakening event in elderly individuals is age-dependent cognitive decline and dementia, with Alzheimer's disease being the chief cause. Understanding the molecular mechanisms underlying Alzheimer's disease and other cognitive deficits is crucial. The regulatory relationship between the mammalian target of rapamycin (mTOR) signaling pathway and Alzheimer's disease, as well as the role of autophagy, is pivotal. Exploring the link between mTOR and autophagy further holds potential for Alzheimer's disease therapy.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Medicine, Research & Experimental
Chayodom Maneechote, Thawatchai Khuanjing, Benjamin Ongnok, Apiwan Arinno, Nanthip Prathumsap, Titikorn Chunchai, Busarin Arunsak, Wichwara Nawara, Siriporn C. Chattipakorn, Nipon Chattipakorn
Summary: The study reveals that modulating mitochondrial dynamics can protect the heart from doxorubicin-induced cardiotoxicity. Inhibiting mitochondrial fission or promoting fusion can alleviate the deterioration of mitochondrial function and dynamic regulation caused by doxorubicin, and mitigate oxidative stress, inflammation, myocardial injury, apoptosis, autophagy, and mitochondrial respiration.
Article
Clinical Neurology
Aurora Veteleanu, Sarah Pape, Kate Davies, Eleftheria Kodosaki, Abdul Hye, Wioleta M. Zelek, Andre Strydom, B. Paul Morgan
Summary: Complement dysregulation is present in individuals with Down syndrome, likely indicating a generalized immune dysregulation state; complement biomarkers differ in individuals with Down syndrome with and without Alzheimer's disease and may be used for diagnosis and/or prediction.
ALZHEIMERS & DEMENTIA
(2023)
Article
Cell Biology
Daniela Impellizzeri, Ramona D'Amico, Roberta Fusco, Tiziana Genovese, Alessio Filippo Peritore, Enrico Gugliandolo, Rosalia Crupi, Livia Interdonato, Davide Di Paola, Rosanna Di Paola, Salvatore Cuzzocrea, Rosalba Siracusa, Marika Cordaro
Summary: This study examined the impact of acai berries on vascular dementia (VaD) in a mouse model. The findings showed that acai berry supplementation could reduce behavioral alteration and hippocampal death caused by VaD, possibly through modulation of Nrf-2 and Beclin-1 molecular pathways. These results suggest that acai berry could be a potential supplementation for the management of VaD in the future.
Article
Neurosciences
Jie Chen, Hai-Jun He, Qianqian Ye, Feifei Feng, Wen-Wen Wang, Yingying Gu, Ruiyu Han, Chenglong Xie
Summary: The main histopathology of Alzheimer's disease is characterized by the accumulation of Aβ plaques and tau neurofibrillary tangles in the brain, likely resulting from interactions among various factors. The link between defective autophagy/mitophagy and AD pathologies is still being investigated, suggesting that targeting autophagy/mitophagy may be a promising anti-AD drug candidate. The complex interplay between autophagy or mitophagy and histopathology in AD implies that inducing autophagy/mitophagy could potentially stop the neurodegenerative course in AD by targeting processes upstream of both NFT and Aβ plaques.
MOLECULAR NEUROBIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Ines C. M. Simoes, Ricardo Amorim, Jose Teixeira, Agnieszka Karkucinska-Wieckowska, Adriana Carvalho, Susana P. Pereira, Rui F. Simoes, Sylwia Szymanska, Michal Dabrowski, Justyna Janikiewicz, Agnieszka Dobrzyn, Paulo J. Oliveira, Yaiza Potes, Mariusz R. Wieckowski
Summary: This study revealed that the progression of non-alcoholic fatty liver disease (NAFLD) involves mitochondrial dysfunction and ROS generation mediated by peroxisomes, rather than excessive mitochondrial ROS production, as previously thought.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Neurosciences
Fan Ye, Anshi Wu
Summary: SIRT1, as a prominent member of sirtuins family, may potentially protect against Alzheimer's disease by regulating mitochondrial biogenesis and autophagy. By affecting neuronal morphology, metabolism, stress responses, and genomic stability, SIRT1 could play a positive role in Alzheimer's disease.
JOURNAL OF ALZHEIMERS DISEASE
(2021)
Review
Pharmacology & Pharmacy
Jia Ke, Qinfang Tian, Qixia Xu, Zhenqin Fu, Qiang Fu
Summary: Alzheimer's disease is an irreversible neurodegenerative disorder characterized by a progressive decline in cognitive function, with mitochondrial dysfunction playing a critical role in its development. While therapeutic strategies targeting mitochondrial dysfunction have shown promise in preclinical studies, clinical trials have made little progress thus far.
DRUG DISCOVERY TODAY
(2021)
Article
Biochemistry & Molecular Biology
Giovanna Trinchese, Fabiano Cimmino, Gina Cavaliere, Angela Catapano, Chiara Fogliano, Adriano Lama, Claudio Pirozzi, Claudia Cristiano, Roberto Russo, Lidia Petrella, Rosaria Meli, Giuseppina Mattace Raso, Marianna Crispino, Bice Avallone, Maria Pina Mollica
Summary: This study investigates the role of the liver in autism spectrum disorders (ASD) and identifies hepatic mitochondrial dysfunction as a potential target for innovative therapeutic strategies for the disease. The findings reveal a link between liver inflammation, oxidative stress, and mitochondrial dysfunction in ASD.
Article
Biochemistry & Molecular Biology
Ana P. Marques, Rosa Resende, Diana F. Silva, Mariana Batista, Daniela Pereira, Brigite Wildenberg, Sofia Morais, Antonio Macedo, Claudia Pais, Joana B. Melo, Nuno Madeira, Claudia F. Pereira
Summary: The study aims to evaluate mitochondrial changes in early stages of bipolar disorder (BD). Fibroblasts derived from BD patients show fragmented mitochondria, altered dynamics, decreased MMP, and increased mitophagy compared to controls. These results suggest that mitochondrial disturbance is an early event in BD pathophysiology that may trigger neuronal changes and brain circuitry modifications.