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Exelon Review Article

 

Exelon also known as rivastigmine tartrate is basically using for the treatment of mild to moderate dementia of Alzheimer’s type usually associated with Parkinson’s disease. The dementia of Parkinson’s disease is characterized by effecting memory retrieval and attention in patients with diagnosis of Parkinson’s disease and it works by preventing the breakdown of the acetylcholine chemical. People suffering from dementia have lower levels of this chemical which is important for the process of memory, thinking and reasoning. The use of Exelon is associated with significant a gastrointestinal adverse reaction which includes vomiting, anorexia weight loss and nausea. For this reason it is important that the usual dose should be started with 1.5 mg of BID and titrated to their maintenance dose.

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1.5 mg 28 caps USD 105.00 Add to Basket
3 mg 28 caps USD 117.00 Add to Basket
4.5 mg 28 caps USD 129.00 Add to Basket
6 mg 28 caps USD 139.00 Add to Basket

Exelon generic (generic - what is it?)

Dosage Packing Price Add to basket
1.5 mg 30 tab ($0.57 per tab) USD 17.00 Add to Basket
1.5 mg 90 tab ($0.50 per tab) USD 45.00 Add to Basket
3 mg 30 tab ($0.63 per tab) USD 19.00 Add to Basket
3 mg 90 tab ($0.59 per tab) USD 53.00 Add to Basket
4.5 mg 30 tab ($0.87 per tab) USD 26.00 Add to Basket
4.5 mg 90 tab ($0.69 per tab) USD 62.00 Add to Basket
6 mg 30 tab ($0.97 per tab) USD 29.00 Add to Basket
6 mg 90 tab ($0.79 per tab) USD 71.00 Add to Basket

rivastigmine in patch formRivastigmine (also known as Exelon) is a drug that has been proved to have extensively beneficial effects on people suffering from Dementia.


DEMENTIA

Dementia comprises of a set of cognitive symptoms that include persistent and progressive impairment of cognitive processes such as attention, memory, language, sleep, and others. It is often accompanied by delusions and visual hallucinations.

One of the main factors which determine the onset of dementia is aging (Bosboom et al., 2004). Dementia is commonly associated with age-related diseases including Alzheimer's disease, Parkinson's disease, and Dementia with Lewy Bodies.

Several studies have shown that the cognitive impairment of dementia are larglely due to the degeneration of cholinergic neurons (these are the neurons that use the neurotransmitter acetylcholine, abbreviated ACh, to help transmit their messages) of the central nervous system (CNS) (Aarsland et al., 2004), a situation prevalent in all three of the above mentioned diseases associated with dementia. Cholinergic degeneration is known to be an age-related phenomenon (Perry et al., 1992).


ACETYLCHOLINE'S ROLE IN DEMENTIA

ACh is of crucial importance for our cognitive processes. It is synthesized in cholinergic neurons by the enzyme choline acetyltransferase from the substrates acetyl coenzyme A and choline. As a response to excitation, neurons can then release ACh which can subsequently be picked up by molecules that reside on adjacent neurons and have special shapes that allow them to receive it. Molecules that can receive neurotransmitters in this way are called receptors, and those that receive ACh are called ACh receptors. Upon receiving ACh, ACh receptors are activated, which triggers further molecular processes which can result in either neuronal inhibition or excitation of the neuron. The excitation of a cholinergic neuron, of course, can lead to further release of ACh, and so on; thus, certain messages can be transmitted along cholinergic neuronal pathways. ACh-induced molecular signaling mechanisms can end with the destruction of ACh, which happens when the enzyme called acetylcholinesterase breaks down (hydrolyses) ACh into the products acetate and choline. Choline can be re-up taken into neurons by special molecules called transporters - it can then be reused for the production of ACh.
In the CNS, cholinergic neuronal pathways are crucially involved in most cognitive processes. This means that abnormalities in the levels of ACh, or in the survival, development, and/or normal functioning of cholinergic neurons, will result in abnormalities of cognition, as in the case of dementia.


RIVASTIGMINE'S THERAPEUTIC EFFECTS

Rivastigmine is believed to exert its therapeutic effects by inhibiting the function of acetylcholinesterase thus compensating for the reduction of cholinergic neuronal function (Bosboom et al., 2004). Rivastigmine has been tested and proved to reduce dementia in patients with Alzheimer's, Parkinson's, and dementia with Lewy bodies.



The chemical structure of rivastigmine
The chemical structure of rivastigmine

Clinical Trials

There have been several studies on the effects of Rivastigmine on human patients with dementia symptoms, and most showed therapeutic effects and relatively few side effects. Most of these studies were open-label trials (i.e. not “blind”), small case series, or studies without placebo controls. There were, however, a few studies that were randomized, placebo-controlled, and involved large populations from various parts of the world. Some of the most important ones (with the largest populations and the longest treatment periods) are mentioned below.

In 1999, R?sler et al. had conducted a randomized, double-blinded, placebo-controlled study on 725 patients suffering from mild to moderately severe Alzheimer's disease. The patients came from centers around Europe and North America. They were administered either placebo, or gradually-increasing doses of Rivastigmine: the Rivastigmine dose was either low (1-4 mg/day) or high (6-12 mg/day). The treatment spanned over 6 months. The results showed significant improvement of cognitive functions.

In 2000, McKeith et al. had conducted a study on 120 patients suffering from mild to moderately severe dementia with Lewy bodies. The patients came from various European countries (UK, Spain, and Italy), they were of both genders and their average age was 74 years. They were treated with gradually-increasing doses of Rivastigmine starting from 6 mg per day and ending to 12 mg per day. The treatment spanned over 20 weeks. The results showed significant improvement of cognitive functions (less anxiety and apathy and less delusions and hallucinations).

In 2004, Emre et al had conducted a randomised, double-blinded, placebo-controlled study on 541 patients diagnosed with Parkinson's disease and with mild to moderately severe dementia. The patients were of both genders, they were at least 50 years old and they coming from various countries around the world. They were administered either 3 mg or gradually increasing to 12 mg of Rivastigmine (Exelon) per day, or placebo. Treatment spanned over 24 weeks. The results of 410 patients who had completed the study showed significant reduction of dementia and improvement of cognitive functions.


Side Effects

The clinical trials reported relatively trivial prevalence of side effects. These mostly included nausea, vomiting, and tremor. Other common side effects reported were diarrhea and anorexia.

Written by: Andreas Apostolides, Pharmacologist.


REFERENCES
• Aarsland D, Mosimann UP, McKeith IG, J 2004, Role of cholinesterase inhibitors in Parkinson's disease and dementia with Lewy bodies, Geriatr Psychiatry Neurol; 17(3):164-71.
• Bosboom JL, Stoffers D, Wolters ECh, 2004, Cognitive dysfunction and dementia in Parkinson's disease, J Neural Transm; 111(10-11):1303-15.
• Emre M, Aarsland D, Albanese A, Byrne EJ, Deuschl G, De Deyn PP, Durif F, Kulisevsky J, van Laar T, Lees A, Poewe W, Robillard A, Rosa MM, Wolters E, Quarg P, Tekin S, Lane R, 2004, Rivastigmine for dementia associated with Parkinson's disease, N Engl J Med; 351(24):2509-18.
• McKeith I, Del Ser T, Spano P, Emre M, Wesnes K, Anand R, Cicin-Sain A, Ferrara R, Spiegel R, 2000, Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study, Lancet; 356(9247):2031-6.
• Perry EK, Johnson M, Kerwin JM, Piggott MA, Court JA, Shaw PJ, Ince PG, Brown A, Perry RH, 1992, Convergent cholinergic activities in aging and Alzheimer's disease, Neurobiol Aging; 13(3):393-400.
• R?sler M, Anand R, Cicin-Sain A, Gauthier S, Agid Y, Dal-Bianco P, St?helin HB, Hartman R, Gharabawi M, 1999, Efficacy and safety of rivastigmine in patients with Alzheimer's disease: international randomised controlled trial, BMJ; 318(7184):633-8.


 

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