Pharmacology: Herbal Therapy With Ginkgo Research Paper

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Health problems that interfere with cognitive functions are always been a concern for patients and medical professionals. This is because of their severe pathological complications that are adding to the growing incidence of the disease. Although various therapeutic strategies have been in progress to curtail this ever-growing problem, considerable interest was centered on herbal therapy. So, the present description is concerned with Alzheimer’s disease and its management with Ginkgo Biloba. Alzheimer’s disease is a neurological disorder as its pathophysiology is strongly believed to originate from the aberrations in the central nervous system due to the detection of markers in the brain tissue from the patients (Dora Dias-Santagata et al., 2007).

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Katharina Schindowski et al. (2006) conducted transgenic studies to investigate the neuropathology of Alzheimer’s disease. They observed hippocampal synaptic transmission and impaired behavior characterized by increased anxiety, delayed learning from 3 months, and reduced spatial memory at 10 months as the pathophysiological disturbances during neurofibrillary degeneration. These changes are believed to originate due to the role of tau protein.

Therefore, it was indicated that cognitive defects in Alzheimer’s disease may be better understood during pathogenic tau aggregation (Katharina Schindowski et al., 2006). These mechanisms may also clearly indicate that cognitive impairments are prevalent in Alzheimer’s disease. Next, although Alzheimer’s disease is a non-inflammatory disease, the involvement of inflammation has also been reported due to the increased production of the proinflammatory cytokine, TNFα and decreased production of the anti-inflammatory cytokine TGFß (Tarkowski et al., 2003). The other change that serves as an important pathological barrier is synaptic dysfunction.

It was reported that amyloid-beta (Aβ) the chief component of senile plaques contributes to the significant reduction in the dynamin 1, a protein that is essential for synaptic vesicle recycling, and hence, for memory formation and information processing.

It may indicate that amyloid beta plays a vital role in the pathogenesis of Alzheimer’s disease (Brent, Robert Vassar &, Adriana Ferreira, 2006). Jose et al. (2005) explored interactions and folding of protein amyloid β-protein Aβ that are regarded as important pathogenic events in the process of neurodegeneration in Alzheimer’s disease. They suggested that the Oligomeric assemblies concerned with the 21-30 region the Aβ may serve as a primary source of neurotoxicity.

It was previously described that the deterioration in Alzheimer’s disease appears to be driven by the neurofibrillary tangles and amyloid plaques (Guilloze et al., 2003). It was revealed that neurofibrillary tangles are more numerous in medial temporal lobe regions and may constitute a pathological substrate for memory loss in AD (Guilloze et al., 2003). Further, several theories have been put forward by scientists to describe the pathology of Alzheimer’s disease.

Schindowski et al. (2008) have shown that the potential factor contributing to the risk is increased neurogenesis during tau hyperphosphorylation and cell cycle events during abnormal tau phosphorylation and tau aggregation preceding neuronal death and neurodegeneration. This study has indicated the role of cell cycle perturbations in the episode of Alzheimer’s disease.

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Sarah and Robert Vassar (2007) reported that the BACE1 enzyme is essential for the generation of β-amyloid. This is because it was found to get elevated in the disease Therefore, the concept of β-secretase(BACE1)biology could provide new insights into the pathogenesis of Alzheimer’s disease. Lee et al. (2007) described that amyloid-beta function which is considered as the vital agent in the pathophysiology has led to the development of the “null hypothesis.”

In contrast “alternate hypothesis” states that amyloid-beta was not an initiating event but rather is secondary to other pathogenic events. This has later developed into more controversy where amyloid-beta was proposed to have a protective function in response to neuronal damage (Lee et al., 2007). Therefore, it can be inferred that these reports have shed significant light on the role of amyloid-beta in the course of Alzheimer’s disease and may suggest further understanding.

Hence, in view of these underlying risk contributors, it is reasonable to assume that the signs and symptoms in Alzheimer’s disease may be of neuropsychiatric origin; and these may include apathy, agitation, anxiety. irritation, dysphoria, disinhibition, and hallucination (Jeffrey, 2005).

It was indicated that these behavioral symptoms are most prevalent in patients with Alzheimer’s disease which would lead to substantial losses in the quality of life for both patients and caregivers (Jeffrey, 2005). It was also reported that patients with Alzheimer’s disease exhibit altered self–awareness in addition to the widely known problem of memory loss (Mimura, 2008).

Hence, a thorough knowledge of symptomology may help in better identifying individuals with Alzheimer’s disease. Further, certain complications are also reported to be associated with Alzheimer’s disease. These are connected to vascular pathology. Xiongwei Zhu et al. (2008) described that vascular abnormalities contribute to the problem of dementia in Alzheimer’s disease. They described vascular factors in association with hypoperfusion that would trigger mitochondrial dysfunction and increased oxidative stress initiating the pathogenic process.

This report has strengthened an earlier description. Luisa Minghetti et al. (2006) described that the depletion of peripheral anti-oxidant defenses would contribute to oxidative stress in Alzheimer’s disease pathogenesis. Therefore the evaluation of total reductive capacity in serum may be beneficial. Therefore, patients with this disorder need to be thoroughly monitored for a better therapeutic understanding.

Finally, it is the prognosis that requires attention. Alan (2006) reported that hormone replacement and the use of non-steroidal anti-inflammatory drugs could help in predicting poor cognitive performance associated with Alzheimer’s disease. Therefore, the utility of hormones and drugs that appear to be reliable markers may have better clinical implications for understanding cognitive impairments. Next, in order to better overcome Alzheimer’s consequences, therapeutic formulations have been modified with the incorporation of herbal extracts. The plant Ginkgo Biloba was identified as a reliable source in this context.

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Previously, it was reported that the extract of Ginkgo biloba, EGb 761 (ginkgolides A and B, myricetin, and quercetin) has neuroprotective effects Aβ1–42-induced synapse damage (Clive Bate, Mourad Tayebi &. Alun Williams, 2008). Therefore, it was indicated that Ginkgo biloba preparations may protect against the synapse damage and the cognitive loss seen during the early stages of Alzheimer’s disease (Clive Bate, Mourad Tayebi &. Alun Williams, 2008).

Further, as oxidative stress is considered as the risk factor of Alzheimer’s disease, it was reported Satoshi Akiba et al.(2004)reported that the leaf extract of Ginkgo Biloba L. has potential antioxidant action through which it executes a variety of pharmacological effects

It can be also inferred that ginkgo extracts may become one of the efficient drugs for treating patients with this Alzheimer’s complaints. Ramassamy, Longpré, and Christen (2007) have provided further insights on the mode of action of Ginkgo biloba extract, EGb 761 with regard to the intracellular pathways. Their report indicated that EGb 761 would exert its anti-amyloidogenic properties or even influence the gene expression through an amyloid cascade.

Earlier scientists have already reported neuronal cell degeneration as the significant characteristic of Alzheimer’s disease (Wenk, 2003). Therefore, understanding the cellular and molecular mechanisms of EGb 761 may help in better studying the pathogenesis. To this end, previous workers have also described that Bilobalide, one of the active constituents found in EGb 761 was found to decrease the frequency of gamma-aminobutyric acid (GABA) uptake inhibitor-induced depolarisations in mouse cortical slices (Davies, Johns, & Jones, 2003).

They highlighted that the ability to reduce excitotoxic glutamate release might be the mechanism behind the neuroprotective properties of Bilobalide. Wang and Chen (2005) further explored the beneficial role of Ginkgo biloba by studying the effect of ginkgolide B in rats. It was revealed that ginkgolide B allowed the Ca2+-dependent release of glutamate-induced by 4-aminopyridine depending on dosage form hippocampal nerve terminals (Wang & Chen, 2005).

Therefore, the above-mentioned research findings may strengthen the possible mechanism of action of Ginkgo Biloba extracts. However, it is also essential to consider the side effects that might create an additional burden to patients with Alzheimer’s disease. Victor, Bernd Wollschlaeger, and Mark Blumenthal (2003) highlighted some of the rare adverse effects of Ginkgo Biloba such as nausea, vomiting, diarrhea, headaches, palpitations, restlessness, weakness, and skin rash. Ginkgo Biloba extracts were also reported to contribute to fatal seizures through neuronal toxicity in patients receiving anticonvulsant therapy (Kupiec & Raj, 2005).

This is because of the induction of Cytochrome P450 enzymes such as CYP2C19 by components of ginkgo which results in subtherapeutic effects of anticonvulsant drugs (Kupiec & Raj, 2005). Therefore, it can be inferred that the ginkgo extracts may interfere with the drug metabolism. Hence, Alzheimer’s patients receiving drug therapy should be cautious while using Ginkgo Biloba supplementation.

But, this may need further clarification. Dugoua et al. (2006) described that poor knowledge regarding the safety indications might increase the risk during pregnancy and lactation. This is due to feeble research evidence indicating that ginkgo leaf has antiplatelet activity, and this study also suggested patients and clinicians develop an awareness of literature on colchicine mixed ginkgo products as they are considered adulterated (Dugoua et al., 2006). Therefore, in view of the side effects, certainly recommended contraindications are that ginkgo products need to be taken with care under the supervision of a qualified health care provider as they may also be associated with the risk of bleeding (Bent et al., 2005).

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Finally, it is the cost factor that is important to consider with regard to the dosage.

It was reported that for a common dosage of 120 mg per day the estimated cost is $15 to $20 for a month’s supply, depending on the brand (Victor S. Sierpina, Bernd Wollschlaeger, & Mark Blumenthal, 2003). Therefore, it can be inferred that Alzheimer’s disease could be managed with Ginkgo Biloba provided there is awareness of its safety and contraindications.

References

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Victor S. Sierpina, Bernd Wollschlaeger, and Mark Blumenthal. (2003). Ginkgo Biloba. Am Fam Physician, 68, 923-6.

Kupiec, T., & Raj, V. (2005). . J Anal Toxicol, 29, 755-8. Web.

Dugoua, J.J., Mills, E., Perri, D., Koren, G. (2006). . Can J Clin Pharmacol, 13, e277-84. Web.

Bent, S., Goldberg, H., Padula, A., Avins, A.L. (2005). . J Gen Intern Med, 20, 657-61. Web.

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IvyPanda. 2021. "Pharmacology: Herbal Therapy With Ginkgo." September 25, 2021. https://ivypanda.com/essays/pharmacology-herbal-therapy-with-ginkgo/.

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