Oxidative Stress Targeting Therapies Study
Background of Oxidative Stress Targeting Therapies Study
Alzheimer's disease (AD) is a chronic neurodegenerative disorder accompanied aging, which is the main cause of dementia. The hallmarks of AD are the aggregation of β-amyloid plaques (Aβ) from cleavage of amyloid precursor protein (APP) processing as well as aggregation of hyperphosphorylated tau and neurofibrillary tau tangles. Elevated reactive oxygen species (ROS) is referred to as oxidative stress. The pathologic progress of AD aggravates oxidative stress, which leads to dysfunction and loss of mitochondria and affects other bioactivities including energy homeostasis, calcium homeostasis, maintenance of cellular architecture, endocytosis, etc. The abnormal bioactivities in patients with AD aggravate the pathologic Aβ and tau accumulation, which in turn exacerbate mitochondrial dysfunction and ROS production. There are no effective therapies that can cure AD, so there is an urgency to contemplate alternative molecular mechanisms to design interventions that can delay or mitigate AD progression. Oxidative stress mechanism of action (MoA) in AD is a promising direction for the development of pharmaceuticals for AD. At present, antioxidant substances against AD in preclinical research include vitamin E, curcumin, coenzyme Q10, idebenone, etc. Besides, antioxidant cocktails therapies have also a positive effect on AD. Creative Biolabs provides a range of in vivo, in vitro, and ex vivo assays, assisting researchers to understand the pathogenesis of AD related to oxidative stress and thus screen therapies targeting oxidative stress.
Oxidative Stress MoA in AD
Oxidative stress MoA in AD is based on the mitochondrial cascade hypothesis. The loss and dysfunction of mitochondria have been detected before the formation of Aβ plaques. The dysfunction of mitochondria associated with age will affect APP processing and thus initiate Aβ aggregation. The energy for biological activities in brain is produced by the oxidation of glucose in mitochondria under aerobic conditions. Glucose metabolism dysfunction related to early mitochondrial dysfunction has been observed in patients with AD, which may directly cause oxidative stress and synaptic dysfunction before Aβ or tau pathology in AD. During the pathologic process of AD, the abnormal cellular metabolism by oxidative stress accelerates the aggregation of pathologic Aβ and tau and in turn increases ROS production. The increased ROS levels cause subsequent DNA damage, neuroinflammation, loss and dysfunction of mitochondrial and synaptic, and abnormal calcium homeostasis.
Fig.1 Schematic illustration of oxidative stress and amyloid β (Aβ) cascade in Alzheimer's disease. (Tadokoro, 2020)
Creative Biolabs offers a full range of services related to oxidative stress targeting therapies study, enabling researchers to study the oxidative stress MoA in AD and therefore explore novel therapeutics against oxidative stress in AD. The assays utilized to study oxidative stress targeting therapies in AD primarily focus on mitochondria, including neuronal mitochondrial activity assay, neuronal mitochondrial membrane depolarization assay, mitochondrial stress assay, parkin mitochondrial recruitment assay, TOM20 mitophagy assay, etc. Our advanced platforms and tools accelerate your research and preclinical drug development progress. If you want to learn more details about oxidative stress targeting therapies study, please don't hesitate to contact us.
Reference
- Tadokoro K.; et al. Prevention of Cognitive Decline in Alzheimer's Disease by Novel Antioxidative Supplements. International Journal of Molecular Sciences. 2020; 21(6): 1974.
