Page 17 - BH-2-2
P. 17

Brain & Heart                                                      Oxidative stress and neurological disorders



            both pharmacological and non-pharmacological therapies   However,  the precise mechanism of cellular physiology
            due to the multifaceted nature of symptoms and the   remains undefined. It is well-established that oxidative
            irreversible damage occurring at multiple levels, such as   stress triggers a cascade of events leading to neuronal
            molecular, cellular, intercellular, and synaptic interactions.   damage. Given the multifaceted nature of these diseases,
            Early diagnosis and understanding of the disease’s etiology   their underlying mechanisms remain elusive. Further,
            can help alleviate symptoms, and numerous clinical trials   comprehensive studies are required to elucidate the signals
            and  preclinical  are  underway. Medications approved  by   induced by oxidative stress that contributes to physiological
            the United States Food and Drug Administration (US   alternations in organs or neurons. Biomarkers of oxidative
            FDA) to reduce symptoms and alleviate disability include   stress hold promise as diagnostic tools and therapeutic
            acetylcholine  inhibitors  such  as  donepezil,  galantamine,   targets for early detection. Antioxidant therapy, along
            rivastigmine, and N-methyl-d-aspartate antagonists.   with a diet rich in antioxidants such as flavonoids,
            These medications are often combined with other drugs,   polyphenolic acids, lipoic acid, and vitamins, can serve as
            such as benzodiazepines for anxiety and acetaminophen   effective therapies. One significant consequence of ROS
            for sleep issues and pain relief. Risperidone is sometimes   production is the overactivation of glutamate receptors.
            prescribed for severe agitation and psychosis. In later   Therapeutic  agents  targeting  these  approaches  show
            stages, Alzheimer’s disease may manifest significant   promise. Administering antioxidant therapy early, before
            neuropsychiatric symptoms and behavioral issues,   neuronal  loss, could prove beneficial. Several intriguing
            including language difficulties, disorientation, and   therapies, such as monoclonal antibodies against protein
            changes in sleep cycle and mood swings.            accumulation, modulation of calcium homeostasis, and
                                                               anti-inflammatory agents, could complement antioxidant
            8.3.3. Antibody-based immunotherapies              therapy in combination treatments. Natural products
            The primary pathological cause of Alzheimer’s disease   are  being  investigated and  modified to  focus  on  more
            reported to date is the abnormal accumulation of   biochemical pathways and enzymatic processing, which
            amyloid plaques. US FDA has approved two monoclonal   may aid in controlling and curing diseases with minimal
            antibodies for use as drugs: aducanumab and lecanemab.    side effects.
                                                         125
            Numerous clinical trials and in vitro studies have reported
            that these are anti-amyloid antibodies capable of slowing   Acknowledgments
            down the deposition of amyloid and reducing cognitive   None.
            decline.  These anti-amyloid  β monoclonal antibodies
                  126
            are administrated intravenously to provide passive   Funding
            immunization. Several other monoclonal antibodies   Nihila Khola is a recipient of a fellowship from the Central
            are still undergoing phase III clinical trials.  All these   University of Haryana. Kareena Moar is a recipient of a
                                                127
            antibodies aim to counteract amyloid accumulation and   junior research fellowship from the Haryana State Council
            halt the cascade of neurodegeneration. These interventions   for Science, Innovation and Technology (HSCIT-3946).
            should decelerate the process of neurodegeneration and   This agency had no role in the interpretation or writing
            functional and cognitive decline.  Recently, four FDA-  the manuscript. The Indian Council of Medical Research
                                       128
            approved monoclonal antibodies targeting amyloid β are   (ICMR), Government of India, is gratefully acknowledged
            in late-phase clinical development, including lecanemab,   by Pawan Kumar Maurya for giving financial assistance
            aducanumab, gantenerumab, and donanemab. All of    (5/10/FR/03/2021-RBMCH).
            these are monoclonal IgG antibodies synthesized to act
            against amyloid aggregates.  Clinical trials investigating   Conflict of interest
                                  129
            these four antibodies provide evidence of the intermediate
            effect of the drug on biomarkers and amyloid removal.   The authors declare no conflicts of interest.
            However, the field of Alzheimer’s disease trials is still   Author contributions
            progressing, and more additional favorable treatments
            for Alzheimer’s disease are likely to be developed in the   Conceptualization: Nikhila Khola, Kareena Moar
            future  (Table 2).                                 Writing-original draft: Kareena Moar
                 130
                                                               Writing-review & editing: Pawan Kumar Maurya
            9. Conclusion and future perspectives
                                                               Ethics approval and consent to participate
            Numerous studies have demonstrated the existence of
            several chronic pathologies induced by oxidative stress.   Not applicable.



            Volume 2 Issue 2 (2024)                         11                               doi: 10.36922/bh.2704
   12   13   14   15   16   17   18   19   20   21   22