Scopolamine as a drug is often used to treat motion sickness. Derivatives of scopolamine
have also found applications as antispasmodic drugs among others. In neuroscience-related research, it
is often used to induce cognitive disorders in experimental models as it readily permeates the bloodbrain
barrier. In the context of Alzheimer’s disease, its effects include causing cholinergic dysfunction
and increasing amyloid-β deposition, both of which are hallmarks of the disease. Hence, the application
of scopolamine in Alzheimer’s disease research is proven pivotal but seldom discussed. In this review,
the relationship between scopolamine and Alzheimer’s disease will be delineated through an
overall effect of scopolamine administration and its specific mechanisms of action, discussing mainly
its influences on cholinergic function and amyloid cascade. The validity of scopolamine as a model of
cognitive impairment or neurotoxin model will also be discussed in terms of advantages and limitations
with future insights.
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Poloxamer 188 (P188) is an FDA-approved biocompatible block copolymer composed of repeating units of poly(ethylene oxide) (PEO) and poly(propylene oxide) (PPO). Due to its amphiphilic nature and high hydrophile-lipophile balance (HLB) value of 29, P188 is used as a stabilizer/emulsifier in many cosmetics and pharmaceuticals preparations. While the applications of P188 as an excipient are widely explored, the data on the pharmacological activity of P188 are scarce. Notably, the neuroprotective potential of P188 has gained a lot of interest. Therefore, this systematic review is aimed to review evidence to support the neuroprotective potential of P188 in CNS disorders. The PRISMA model was used, and five databases (Google Scholar, SCOPUS, Wiley Online Library, ScienceDirect, and PubMed) were searched with relevant keywords. The research resulted in 11 articles, which met the inclusion criteria. These articles described the protective effects of P188 on traumatic brain injury or mechanical injury in cells, neurotoxicity, Parkinson’s disease, Amyotrophic lateral sclerosis (ALS), and ischemia/ reperfusion injury from stroke. All the articles were original research in experimental or pre-clinical stages using animal models or in vitro systems. The reported activities demonstrated the potential of P188 as a neuroprotective agent in improving CNS conditions such as neurodegeneration.
Epilepsy is a severe neurological disorder involving 70 million people around the globe. Epilepsy-related neuropsychiatric comorbidities such as depression, which is the most common, is an additional factor that negatively impacts the living quality of epilepsy patients. There are many theories and complexities associated with both epilepsy and associated comorbidities, one of which is the gut-brain-axis influence. The gut microbiome is hypothesized to be linked with many neurological disorders; however, little conclusive evidence is available in this area. Thus, highlighting the role will create interest in researchers to conduct detailed research in comprehending the influence of gut-brain-axis in the manifestation of depressive symptoms in epilepsy. The hypothesis which is explored in this review is that the gut-brain-axis do play an important role in the genesis of epilepsy and associated depression. The correction of this dysbiosis might be beneficial in treating both epilepsy and related depression. This hypothesis is illustrated through extensive literature discussion, proposed experimental models, and its applicability in the field. There is indirect evidence which revealed some specific bacterial strains that might cause depression in epilepsy.
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