Neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are becoming more frequent as the age increases. Contemporary therapies provide symptom resolution instead of targeting underlying pathological pathways. Consequently, there is considerable heterogeneity in response to treatment. Research has elucidated multiple potential of pathophysiological mechanisms contributing to neurodegenerative conditions, among which oxidative stress pathways appear to be suitable drug targets. The oxidative stress pathway has given rise to numerous novel pharmacological therapies that may provide a new avenue for neurodegenerative diseases. For example, SKQ (plastoquinone), MitoVitE, vitamin E, SOD mimic, MitoTEMPO (SOD mimetic), and bioactive molecules like curcumin and vitamin C have indeed been examined. To better understand how oxidative stress contributes to neurodegenerative diseases (such as Alzheimer’s and Parkinson’s), we analyzed the medicinal qualities of medicines that target markers in the cellular oxidative pathways. The specific pathway by which mitochondrial dysfunction causes neurodegeneration will require more investigation. An animal study should be carried out on medications that tackle cellular redox mechanisms but are not currently licensed for use in the management of neurodegenerative conditions.

Stroke is one of the leading causes of disability, dementia, and mortality worldwide. It is a medical emergency characterized by the interruption or reduction of the flow through brain blood vessels, leading to poor perfusion of brain tissue [1]. The three main types of stroke are ischemic stroke, hemorrhagic stroke, and transient ischemic attack. Whereas the global age-standardized stroke mortality rates reduced remarkably between the years 1990 and 2016, the opposite took place in Africa, which has witnessed a rate of about 316 per 100,000 persons per annum, with a prevalence of 1460 per 100,000 persons and a mortality incidence of >80% within 3 years of the disease onset [2]. About 70% of all deaths and 87% of disabilities associated with a stroke episode between 1970 and 2010 were linked to

Introduction Alzheimer's disease (AD) is a leading cause of dementia around the globe. Its pathogenesis is characterized primarily by the extracellular deposition of amyloid β peptides and intracellular neurofibrillary tangles. Despite the significant investments in neurological research, the exact molecular mechanism of AD pathogenesis is still not fully elucidated. Several studies converge on a hypothesis that pathogenic microbes might play a role in AD progression. Although this hypothesis has been considered relatively weak for decades, it has recently received considerable attention due to increasing evidence on the association between microorganisms and AD. There is a lack of experimental and scientific arguments conveying that these microorganisms engender cognitive and neuropathological deficits and modifications specific to AD, challenging the theory that it could be an infectious neurological disease. This review focuses on recent advances in the infection hypothesis and provides an overview of new findings portraying the significance of pathogenic microbes in AD and the challenges confronting the validity of the hypothesis. Methodology Data were collected from medical journals published on PubMed, Ovid MEDLINE, ScienceDirect, and Embase bibliographical databases with a predefined search strategy. All articles considering neurological disorders, especially AD associated with infectious diseases, were included. Results This work focused on providing an overview of new findings around the relationship between microorganisms and AD, challenges facing the validity of the theory, and recommendations on how the scientific community can best develop alternative approaches to address the pathophysiology of AD. Conclusion While many studies reinforce the suspicion of an infectious etiology of AD, it is important to note that it is yet not validated how microorganisms’ presence in the brain can develop AD due to the limited available evidence. Certainly, ground‐breaking work is mandatory in this field of research, and these reports so far warrant a thorough investigation into how a chronic infection may remain silent while progressing its neuroinflammation. Amid this uncertainty arises the hope that many researchers will take on this challenge and join this endeavor to benefit AD patients worldwide.