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Nervous System
Published in Joseph D. Bronzino, Donald R. Peterson, Biomedical Engineering Fundamentals, 2019
Amyloid-beta (AB) is the major substance implicated in the progression of AD. Large amounts of this peptide due to overproduction, lack of degradation, or other factors lead to the formation of senile plaques. eir presence may trigger the release of cytochrome C, which is associated with apoptosis (cell death) and neurodegeneration. (PD also involves amyloids that aggregate and participate in the direct or indirect loss of synapses and neurons.) Other studies point to excessive amounts of glutamate in the extracellular uid. eir presence is thought to very rapidly inhibit the transport of molecules from the cell body to the end terminal of the axon, therefore leading to the loss of synapses-the end result of AD. us, chemical synaptic input is stopped and the ability of the person to perform certain functions is greatly inhibited.
Nanostructured Drug Delivery of Nutraceuticals for Counteracting Oxidative Stress
Published in Bhupinder Singh, Minna Hakkarainen, Kamalinder K. Singh, NanoNutraceuticals, 2019
Shobhit Kumar, Bharti Gaba, Jasjeet K. Narang, Javed Ali, Sanjula Baboota
CoQ10 is a well-known endogenous antioxidant and also has anti-amyloidogenic activity. Both of these properties help in the treatment of disorders such as diabetes mellitus, CNS pathologies, and cancer. Generally, it is involved in energy production where it acts as a cofactor. It has the potential to block apoptosis mechanism of cell death and could be useful in the management and prevention of neuroprotective disorders (Young et al., 2007; Belhaj et al., 2012). Furthermore, it was investigated that it also delayed the amyloid beta-protein toxic effects, which makes its role useful in the prevention of Alzheimer’s disease (Young et al., 2007). In spite of its usefulness, poor oral bioavailability is a problem in clinical development of CoQ10, which is mainly caused by its poor aqueous solubility (<0.25 μg/mL). There is need to prepare carriers capable of improving CoQ10 solubility and stability. Different strategies have been applied for increasing CoQ10 solubility, such as liposomes, SNEDDS, and NLCs.
Breathomics and its Application for Disease Diagnosis: A Review of Analytical Techniques and Approaches
Published in Raquel Cumeras, Xavier Correig, Volatile organic compound analysis in biomedical diagnosis applications, 2018
David J. Beale, Oliver A. H. Jones, Avinash V. Karpe, Ding Y. Oh, Iain R. White, Konstantinos A. Kouremenos, Enzo A. Palombo
Breath testing techniques such as electronic nose devices have been used to detect and differentiate the patients suffering from Alzheimer’s and Parkinson’s diseases (Bach et al., 2015). The study used an E-nose (for VOC sampling) in conjugation with ion mobility spectrometry. The sample analysis was confirmed by use of an existing standard enzyme-linked immunosorbent assay (ELISA) technique for the detection of the possible causative agent, amyloid beta (Aβ). The predictability of the conducted tests to detect Alzheimer’s and Parkinson’s diseases was reported to be ca. 94%. Likewise, other chronic degenerative diseases such as liver cirrhosis can be detected at a comparatively early stage by VOC sample analysis (Pijls et al., 2016). The experiment involved the detection of signature metabolome profiles for chronic liver disease (CLD) and compensated cirrhosis (CC). GC-MS analysis was performed on exhaled breath collected in Tedlar® bags. Approximately 11 discriminatory metabolites were observed for CLD and CC. These metabolites comprised propanoic acid, octane, terpene, dimethyl sulfoxide (DMSO, increased), methyl butanal and hexadecanol (depleted), possibly caused by impaired cytochrome P450 detoxification mechanisms in the liver (Pijls et al., 2016).
Vitamin E modified polyamidoamine dendrimer for piperine delivery to alleviate Aβ1–42 induced neurotoxicity in Balb/c mice model
Published in Journal of Biomaterials Science, Polymer Edition, 2023
Ajit Singh, Debarati Rakshit, Ankit Kumar, Awanish Mishra, Rahul Shukla
Alzheimer’s disease (AD) is related to the autonomous neurofibrillary deterioration of muscarinic neurons in brain. The major neurodegeneration affected area in the brains are cerebral cortex and hippocampus [1]. Amyloid beta (Aβ) proteins monomers in response to self-recognition assembles into oligomers which ultimately transform into neurotoxic aggregated plaques. These aggregates mostly accumulate at extra- neuronal locations as a result of increased Aβ deposition and decreased clearance from brain [2]. In response Aβ1-42 extrinsic deposition glial cells releases reactive oxygen species (ROS) initiates programmed cell death in neurons which leads to dementia [3]. Currently N-methyl D-aspartate antagonist or acetylcholine esterase (AChE) inhibitor therapy provides temporary relieves to symptoms of AD patients [4]. Therefore, there is a requirement for strategies to attenuate neurotoxicity in AD models on targets, including Aβ aggregates disaggregation, scavenging ROS, and reestablishing normal acetylcholine levels in brain. Therefore such therapeutic agent or multifunctional nanomedicine is required which have characteristics of all three strategies mentioned above.