Review
Neurosciences
Russell H. Swerdlow
Summary: Viable hypotheses about Alzheimer's disease must consider its age-dependence, commonality, association with specific biological factors, connection with various changes in the body, and systemic features. Mitochondria and factors influenced by mitochondria may link these different characteristics. The mitochondrial cascade hypothesis provides a straightforward explanation and accumulating data support its validity. While alternative hypotheses may also explain mitochondria-related phenomena, the primary mitochondrial cascade hypothesis will continue to evolve and attract interest.
JOURNAL OF ALZHEIMERS DISEASE
(2023)
Review
Biochemistry & Molecular Biology
German Plascencia-Villa, George Perry
Summary: The deterioration of brain cells in neurodegenerative diseases is accompanied by mitochondrial dysfunction. Current therapies for Alzheimer's and Parkinson's disease mainly focus on maintaining neurotransmitters and managing symptoms, with limited effectiveness in stopping or reversing the disease. This article discusses alternative molecular targets for treating neurodegeneration, such as regulating calcium ion transport, protein modification, glucose metabolism, antioxidants, metal chelators, vitamin supplementation, and mitochondrial transference. Some of these targeted therapies have shown promise in preclinical and animal studies, and are expected to have positive outcomes in clinical trials.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Geriatrics & Gerontology
Qixue Wang, Mengna Lu, Xinyu Zhu, Xinyi Gu, Ting Zhang, Chenyi Xia, Li Yang, Ying Xu, Mingmei Zhou
Summary: Anxiety in early life is linked to an increased risk of Alzheimer's disease (AD) later in life. Mitochondria dysfunction caused by anxiety-triggered oxidative stress might be a possible mechanism that connects early life anxiety to AD. Mitochondria play crucial roles in maintaining brain function, and disruptions in glucose homeostasis can lead to oxidative stress. Targeting mitochondria to reduce oxidative stress may prevent or delay the onset of AD in individuals with anxiety disorders.
Article
Biochemistry & Molecular Biology
Kerry C. Ryan, Jocelyn T. Laboy, Kenneth R. Norman
Summary: Mitochondrial dysfunction and oxidative stress are major contributors to neurodegenerative diseases. This study reveals that elevated mitochondrial calcium levels, rather than cytosolic calcium levels, lead to increased reactive oxygen species (ROS) production and subsequent neurodegeneration in sel-12 mutants. The study also identifies mTORC1 signaling as a critical factor in sustaining high ROS levels in sel-12 mutants.
Review
Biochemistry & Molecular Biology
Anamaria Jurcau
Summary: With an aging population, the incidence of neurodegenerative diseases is on the rise, and current treatments primarily focus on symptom relief. Preventative measures such as a healthy lifestyle and avoidance of oxidative stress are recommended.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Biochemistry & Molecular Biology
Inigo San-Millan
Summary: The role of mitochondrial function in health and disease has gained increasing recognition in recent years. Mitochondrial dysfunction and disruptions of cellular bioenergetics have been found to be present in various prevalent diseases, such as type 2 diabetes, cardiovascular disease, metabolic syndrome, cancer, and Alzheimer's disease. However, the causes and mechanisms of mitochondrial dysfunction in these diseases are still not fully understood, making it a significant medical challenge. Advances in our understanding of cellular metabolism and genetics offer promise in unraveling the mysteries of mitochondria and developing therapeutic treatments.
Review
Biochemistry & Molecular Biology
Gurjit Kaur Bhatti, Anshika Gupta, Paras Pahwa, Naina Khullar, Satwinder Singh, Umashanker Navik, Shashank Kumar, Sarabjit Singh Mastana, Arubala P. Reddy, P. Hemachandra Reddy, Jasvinder Singh Bhatti
Summary: Mitochondria, the powerhouses of cells, play a vital role in maintaining normal cell functioning and human health. Dysfunctional mitochondria can lead to various diseases, affecting organs with high energy demand. Drugs or compounds targeting mitochondria are considered effective and safe for treating these diseases.
BIOMEDICAL JOURNAL
(2022)
Article
Cell Biology
Doris Chen, Wanjia Yu, Laura Aitken, Frank Gunn-Moore
Summary: This study identifies Willin/FRMD6 as a potential risk gene for Alzheimer's disease (AD), and demonstrates the direct effects of A beta on its expression. The study also reveals mitochondrial oxidative stress as a novel mechanism underlying the role of Willin/FRMD6 in AD pathogenesis. Additionally, the study shows that knockdown of Willin/FRMD6 leads to mitochondrial dysfunction and upregulation of ERK1/2 signaling, which are key early features of AD. Increasing Willin/FRMD6 expression may serve as a therapeutic strategy for protecting against A beta-induced mitochondrial and neuronal dysfunction.
Article
Chemistry, Multidisciplinary
Qian Zhang, Qingxiang Song, Renhe Yu, Antian Wang, Gan Jiang, Yukun Huang, Jun Chen, Jianrong Xu, Dayuan Wang, Hongzhuan Chen, Xiaoling Gao
Summary: Mitochondrial dysfunction is a key factor in neurodegenerative diseases like Alzheimer's disease (AD). The dysregulation of mitochondrial calcium ion homeostasis and mPTP activation contribute to mitochondrial dysfunction in AD. A therapeutic strategy that combines a Ca2+ antagonist and siRNA to regulate mPTP is proposed. The treatment efficiently halts mitochondrial dysfunction and alleviates AD neuropathology.
Review
Biochemistry & Molecular Biology
Nerea Mendez-Barbero, Jorge Oller, Ana B. Sanz, Adrian M. Ramos, Alberto Ortiz, Marta Ruiz-Ortega, Sandra Rayego-Mateos
Summary: Cardiovascular disease (CVD) often accompanies chronic kidney disease (CKD), and patients with both conditions have an increased risk of all-cause mortality ranging from 20% to 500%. Maintaining mitochondrial homeostasis appears to be a promising therapeutic strategy for the cardio-renal syndrome (CRS). This review explores the role of mitochondrial dysfunction in cardiovascular and renal diseases and how it may guide the development of novel therapeutic strategies for CRS.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Maria Carolina Jurcau, Felicia Liana Andronie-Cioara, Anamaria Jurcau, Florin Marcu, Delia Mirela Tit, Nicoleta Pascalau, Delia Carmen Nistor-Cseppento
Summary: Alzheimer's disease is a common form of dementia with increasing incidence and mortality rates. Current approved drugs for treatment have little effect on disease progression. Research has identified oxidative stress, mitochondrial dysfunction, and chronic neuroinflammation as key factors, pointing to potential therapeutic targets. Novel molecules and cell-based therapies have shown efficacy in vitro and animal models, but further research is needed for clinical translation.
Article
Neurosciences
Mohd Salman, Mohd Akram, Mohd Shahrukh, Tauheed Ishrat, Suhel Parvez
Summary: This study explored the effects of pramipexole (PPX) on cognitive impairments, oxidative damage, and mitochondrial dysfunction in Aβ(1-42) rats. The results showed that PPX improved cognitive impairments, attenuated oxidative damage, and restored mitochondrial function. PPX exerted its protective effects by reducing oxidative stress, enhancing antioxidant capacity, and improving mitochondrial dynamics.
Review
Neurosciences
Shiveena Bhatia, Rishi Rawal, Pratibha Sharma, Tanveer Singh, Manjinder Singh, Varinder Singh
Summary: Alzheimer's disease is a major cause of senile dementia, characterized by accumulation of plaques and tangles in the brain leading to neurodegeneration and cell death, along with other pathological features such as abnormal microvasculature and increased beta-amyloid production. Mitochondrial Dysfunction (MD) is implicated in all associated AD pathologies, with evidence suggesting its involvement in the progression of neurodegeneration in AD.
CURRENT NEUROPHARMACOLOGY
(2022)
Article
Neurosciences
Fatemeh Nabavi Zadeh, Maryam Nazari, Abdollah Amini, Soheila Adeli, Amir Barzegar Behrooz, Javad Fahanik Babaei
Summary: The study aimed to investigate the neuroprotective action of alpha-tocopherol on memory-impaired rats induced by icv-STZ. The results demonstrated that alpha-tocopherol could alleviate cognitive impairment, reduce oxidative stress and mitochondrial dysfunction, and correct neurodegenerative defects.
FRONTIERS IN NEUROSCIENCE
(2023)
Article
Neurosciences
Jasvinder Singh Bhatti, Kavya Thamarai, Ramesh Kandimalla, Maria Manczak, Xiangling Yin, Subodh Kumar, Murali Vijayan, P. Hemachandra Reddy
Summary: The study found that SS31 treatment in diabetic mice could reduce mitochondrial dysfunction, restore mitochondrial function, lower lipid peroxidation, and increase ATP production, serving as a potential protective measure.
MOLECULAR NEUROBIOLOGY
(2021)