The basis for tracking drug safety in actual medical practice and the identification of unexpected side effects that weren't identified at the time of market authorization. Alzheimer's and Parkinson's patients are more likely to have negative drug reactions due to the complexity of brain activity and therapy. Anti-Alzheimer and anti-Parkinson drug pharmacovigilance is further hampered by the fact that each patient requires unique therapy. It's much more difficult when there's a lack of comprehensive safety and risk data for a medicine, which can happen with novel compounds or treatments for children. There is no known treatment for this condition. One of the most significant concerns that Alzheimer and Parkinson patients confront during their sickness is the side effects or no cure of their treatment. As there is limited approved researches and approved drug for treatment (not cure) due to complications and safety monitoring or drugs going through clinical trials.
A neurological condition called Alzheimer's disease results in the loss and atrophy of brain cells. The most common form of dementia, Alzheimer's disease is characterized by a progressive decline in cognitive, behavioral, and social skills that reduces a person's ability to function independently. Medication may reduce the severity of symptoms or offer momentary respite. These medications can help people with Alzheimer's disease maintain their independence and occasionally function better. There are numerous programs and services available for people with Alzheimer's. (Albert et al., 2011). Parkinson's disease (PD) is the second most prevalent movement condition among neurodegenerative disorders. An essay on the shaking palsy by James Parkinson, published in 1817, was the first to describe it. Later, in the late 1800s, prominent French neurologist Jean-Martin Charcot elaborated on the disease. The greatest significant risk factor for Parkinson's disease is also senior age; about 1-2 percent of those over 65 worldwide have this progressively worsening degenerative disorder. 90% to 95% of cases of Parkinson's disease are idiopathic, or without known cause, and the remaining 5% are familial (5-10 percent). [...]
TABLE OF CONTENT
CHAPTER A - INTRODUCTION
CHAPTER B - LITERATURE REVIEW
B.1. UNDERSTANDING PARKINSON AND ALZHIEMER’S AND WHY IT IS HARD TO TREAT
B.2. BEST TREATMENT OF PARKINSON DISEASE AVAILABLE IN MARKET
B.3. BEST TREATMENT OF ALZHIEMER DISEASE AVAILABLE IN MARKET
B.4. LEGAL FRAMEWORK AND LEGAL BASIS FOR PARKINSON
B.5. LEGAL FRAMEWORK AND LEGAL BASIS FOR ALZHIEMER
CHAPTER C - RESEARCH METHODOLOGY
REFERENCING
CHAPTER A- INTRODUCTION:
The basis for tracking drug safety in actual medical practice and the identification of unexpected side effects that weren't identified at the time of market authorization. Alzheimer's and Parkinson's patients are more likely to have negative drug reactions due to the complexity of brain activity and therapy. Anti-Alzheimer and anti-Parkinson drug pharmacovigilance is further hampered by the fact that each patient requires unique therapy. It's much more difficult when there's a lack of comprehensive safety and risk data for a medicine, which can happen with novel compounds or treatments for children. There is no known treatment for this condition. One of the most significant concerns that Alzheimer and Parkinson patients confront during their sickness is the side effects or no cure of their treatment. As there is limited approved researches and approved drug for treatment (not cure) due to complications and safety monitoring or drugs going through clinical trials.
A neurological condition called Alzheimer's disease results in the loss and atrophy of brain cells. The most common form of dementia, Alzheimer's disease is characterized by a progressive decline in cognitive, behavioral, and social skills that reduces a person's ability to function independently. Medication may reduce the severity of symptoms or offer momentary respite. These medications can help people with Alzheimer's disease maintain their independence and occasionally function better. There are numerous programs and services available for people with Alzheimer's. (Albert et al., 2011). Parkinson's disease (PD) is the second most prevalent movement condition among neurodegenerative disorders. An essay on the shaking palsy by James Parkinson, published in 1817, was the first to describe it. Later, in the late 1800s, prominent French neurologist Jean-Martin Charcot elaborated on the disease. The greatest significant risk factor for Parkinson's disease is also senior age; about 1-2 percent of those over 65 worldwide have this progressively worsening degenerative disorder. 90% to 95% of cases of Parkinson's disease are idiopathic, or without known cause, and the remaining 5% are familial (5-10 percent). Clinically, Parkinson's disease can be identified by motor issues such bradykinesia (difficulty starting movement), tremor (pill-rolling action of the forearm), and muscle stiffness, as well as by secondary symptoms like hunched posture, difficult walking, mask-like face, and sialorrhea (Albert et al., 2011). Non-motor symptoms include things like depression, constipation, pain, genitourinary issues, sleep issues, emotional and linguistic abnormalities, dementia, cognitive impairments, muscle spasms, dystonia, tiredness, and a lack of vitality. (Cummings.,2019). The loss of dopamine neurons in the nigra pars compacta causes a lack of dopamine in the striatum and an accumulation of the protein -synuclein, which culminates in the formation of Lewy bodies. This is the main pathogenic hallmark of Parkinson's disease. Despite the fact that it is uncertain what function these Lewy bodies have in the pathogenesis of Parkinson's disease, misfolded -synuclein has been discovered to be a significant component of both radiating filaments in the condition. In Parkinson's disease, oxidative stress, excitotoxicity, mitochondrial dysfunction, neuroinflammation, protein aggregation, phosphorylation, genetic disorders, and toxins are among the additional pathogenic pathways linked to the death of dopaminergic cells (Nagai et al.,2012).
CHAPTER B - LITERATURE REVIEW
UNDERSTANDING PARKINSON & ALZHEIMER’S AND WHY IT IS HARD TO TREAT THIS DISEASE
Parkinson's disease pharmacotherapeutic targets Disease is a complex condition characterized by the activation of many biochemical processes in dopaminergic neurons. MPTP toxicity, changes in levels of neurotransmitters, oxidative stress, glutamate excitotoxicity, mitochondrial dysfunction, neuro inflammation, changes in gene regulation, protein aggregation, and heavy metal poisoning are among these mechanisms.
Regardless of the fact that this is currently the best model for symptomatic of Parkinson's disease which is movement and motor disorder, lengthy use of levodopa has indeed been connected to the concept of potentially severe motor complications like as reflex oscillations with levodopa-induced dyskinesias, which affect about 30-35 percent of patients after just 2 years of treatment. Many new neuroprotective compounds are being researched to avoid the difficulties associated with levodopa. These agents use various unique mechanisms of action to achieve their goals. (Jellinger and Attems,2022)
In the 1960s, the parent of dopamine, levodopa, was developed as a therapy for Parkinson's disease and has always been the most effective therapeutic drug for the disease in 2020. Other dopaminergic medications, including as inhibitors of dopamine metabolism and dopamine receptor agonists, have since been utilized, although they are often less well tolerated and less effective. As a result, improved medicines, particularly disease-modifying medications, are urgently needed. However, the absence of robust biomarkers for diagnosing PD and identifying prodromal illness, which will also allow for therapy before considerable neuronal loss has occurred, as well as the demand for suitable pre-clinical disease models for testing such drugs, presents challenges to drug development. (Carrillo and Vellas.,2003)
It is such a diverse disorder that the name "Parkinson's diseases" has been advocated as a better way to characterized the many clinical entities. Many various subtype categorization systems have been developed, raising issues regarding which are the most helpful and what implications they have for future study. Despite substantial scientific efforts to categories Parkinson's disease and evidence that subtypes are linked to disease progression, subtypes have only been included in a few therapeutic trials. They are linked to etiology prognosis, or therapy response. If they do, they might be important tools for improving research methodologies and, as a result, finding a cure or improved treatments, as well as assisting us in counselling patients and directing existing medicines. Only by include subgroups in clinical research studies can these prospects be realized. We will examine the goal of subtyping, the present level of knowledge on PD subtypes, and how subtypes may be utilized most effectively in research on the aetiology, progression, and therapy of PD in this study. Parkinson's disease is characterized by cell damage in the substantia nigra, notably in the medial region of something like the par’s compacta (Nagai et al.,2012). When opposed to almost the similar region in unhealthy individuals, that area of the brain had lost 50- 70percent of the overall of its nerve cells by the moment of death. The initial places of degenerative alterations in Parkinson's disease have been the medulla oblongata or pontine tegmentum, and also the olfactory bulb. People have no symptoms in the early stages. The substantia nigra, as well as parts of the midbrain and basal forebrain, become affected as the illness progresses. Finally, pathogenic alterations manifest themselves in the neocortex. This neocortex undergoes pathogenic alterations. This diseased stage is founded on the spread of Lewy bodies. The presence of Lewy bodies is a pathogenic feature of Parkinson's disease. They're a-synuclein-immunoreactive aggregates made up of several different of neural filament and proteolytic proteins. Ubiquitin, a heat shock protein that assists in the destruction of other proteins, is one of them, suggesting that this parkin protein is required for the development of something like the Lewy body (Albin and Frey.,2003). Parkin has been found to cause Lewy bodies by increasing ubiquitin binding to another proteins, notably the a-synuclein interacting protein synphilin-1. 4 Lewy bodies are merely a pathogenic signature (DLB) for Parkinson's disease and neurodegenerative disorders, but not for any other neurodegenerative illnesses. The ubiquitin-proteasome system (UPS) is being studied as a potential participant in cell death as a result of the discovery of single gene aberrations in Parkinson's disease (PD). The UPS is essential for the intracellular processes that keep cells alive, including cytoplasmic proteolysis. It accomplishes this by eliminating unneeded proteins from the cell. An abnormal protein aggregation, including that of a-synuclein, a crucial part of Lewy bodies, happens when the UPS malfunctions. The olfactory bulb is one of the first areas where LB accumulates in Parkinson's disease in its early stages. The olfactory bulb is one of the first areas where LB accumulates in Parkinson's disease in its early stages. It is particularly noteworthy because one of the initial clinical signs of Parkinson's disease is typically a change in smell or taste, supporting the concept that the creation of LB is crucial for the activation of circumstances that can result in neuronal malfunction and death. Similar circumstances apply to Alzheimer's disease, which has no known cure and cannot be stopped as it spreads across the brain. Dehydration, starvation, or infection are complications from a significant loss of brain function that can result in mortality in more advanced stages of the illness (Albin and Frey.,2003).
Alzheimer's disease is characterized by memory loss. An inability to recall earlier conversations or activities is one of the early signs of dementia. As the illness progresses, memory issues get worse and other symptoms show up. Patients with Alzheimer's may initially experience memory loss and trouble structuring their thoughts. Your family or friends may have noticed how the symptoms get worse over time. In an effort to understand the causes of Alzheimer's disease, researchers are examining the role of two proteins: Plaques The brain has a smaller protein called beta-amyloid. When they accumulate, these fragments seem to have an adverse effect on neurons and impair cell-to-cell communication. These clusters combine to create amyloid plaques, which also contain additional cellular waste. Tangles. The internal support and transport mechanism of neurons uses tau proteins to carry nutrition and other crucial elements. Neurofibrillary tangles are collections of tau proteins that have changed structure and are seen in Alzheimer's disease. Tangles damage cells and interfere with the transport mechanism. (Ballard et al.,2013)
Best Treatment of Parkinson’s Disease available in market First line levodopa treatment
For more than a fourth, levodopa in combination with a distal decarboxylase blocker has indeed been considered as the gold standard inside the treatment of Parkinson's disease. It has been the most effective medicine therapy in very many aspects. However, the advantages gained frequently come at a cost. Levodopa medication for a long time generally has incapacitating withdrawal symptoms. Dopamine antagonists dyskinesias develop at a rate of 10% per year on average after initiating levodopa, while this index is greater in earlier onset people. The period of the illness and the dosage of levodopa supplied are the primary causes of motor fluctuations, whereas the duration of levodopa therapy is the chief reason of dyskinesias. (Lu and MacDermid.,2019)
First line dopamine agonist treatment
In the U.K. there are six oral dopamine agonists. Rotigotine is a subcutaneous patch that contains a non-ergot adrenergic. Every one of these drugs activate the post-synaptic antipsychotic drugs. Dopamine agonists were originally licensed for its use in people who were taking levodopa and had developed Parkinson's disease. Their acceptance as first-line treatments were based on their ability to improve motor symptoms while also delaying the use of levodopa and the development of levodopa problems. Monotherapy experiments have been conducted with dopamine agonists including levodopa. Bromocriptine monotherapy postponed the development of dyskinesias when contrasted to levodopa treatment and had no impact on the beginning of motor oscillations, according to the first study, which was done in the 1980s. In compared to levodopa, studies of the more recently produced dopamine agonists demonstrated a significant reduction in the onset of motor difficulties in those who started taking the agonist alone. Treated patients with levodopa had better UPDRS scores (parts 2 and 3) than those treated with dopamine agonists in published studies of ropinirole and pramipexole monotherapy, even though patient and physician assessments for the two arms were equivalent during the trials. The levodopa and placebo groups had the same quality of life (QoL) outcome indicators during the four years of something like the calm -pd study. Whereas disorientation & hallucinations are much more likely than it does with levodopa individually, systemically dopamine agonist has such a comparable pharmacokinetic profile to levodopa. (Souza et al.,2021) The primary treatment concern in Parkinson's is as follows: antipsychotic medications produce less motor difficulties and then the same QoL ratings, although at the cost of more adverse effects and far worse efficacy as determined either by UPDRS. Although there is a widespread assumption that now the risk of adverse effects from dopa agonist monotherapy is higher in senior individuals, Studies with both the stronger agonists have shown that such drugs are so well absorbed in those over 75 years old. However, as previously stated, while utilizing agonists in the elderly, more vigilance is essential. (Heiko Braak et al.,2009)
First-line MAO-B inhibitors-
Since the DATATOP trial, MAO-B inhibitors became extensively employed due to their shown effectiveness in symptom relief and assumed 'neuroprotective' impact. However, a current finding by the U.k Parkinson's Disease Research, which followed over 700 participants with moderate early PD, discovered that that use selegiline and levodopa had a considerably greater mortality rate compared people taking levodopa or bromocriptine separately. This conclusion was not supported by subsequent research, which revealed the contrary, namely, a potential decrease in mortality (Broich et al.,2011). MAO-B drugs were proven to reduce impairment, the need for levodopa, as well as the prevalence of motor oscillations in a recent show of seventeen randomized studies including 3525 patients, with no negative side effects or increased mortality. That most of these trials were short-term and didn't equate selegiline to a dopamine agonist as an initial therapy. MAO-B inhibitors, but at another hand, may have a function with first monotherapy in Depressed patients. Rasagiline, a new MAO-B inhibitor, has been shown to be effective in both diagnosis of early illness investigations Using TEMPO provided results which were compatible with such an illness effect, albeit, just like the drug studies, further research needs to be done to prove a neuroprotective benefit. (Heiko Braak et al.,2009)
COMT inhibitors-
Entacapone is indeed a central catechol-O-methyltransferase COMT antagonist that works in tandem with AADC antagonists to block catechol-O-methyltransferase COMT. The introduction of entacapone enhances the serum half-life of levodopa by 60 per cent it after every dosage, assuming overall dosage stays unaltered. Tolcapone, too, increases the ^ of levodopa in a dosage-dependent manner, regardless of the fact that it is administered independently of the levodopa dosing regime. (Feldman et al.,2020) When entacapone or tolcapone is added to levodopa/AADC binding site treatment, it hinders COMT, along many of the key enzymes in dopamine biotransformation, resulting in higher but rather longer- lasting dopaminergic in the serum and central nervous system even than carbidopa on its own, resulting in better motor function but a longer time of antiparkinsonian activity.
Inhibition of COMT has a number of side effects, levodopa serum consent. are less likely to fluctuate, keeping levels inside the therapeutic window and extending the effect of each dosage of levodopa. Tolcapone was previously discontinued due to allegations of hepatotoxicity, however it was subsequently reintroduced following tight monitoring protocols for limited usage. Entacapone, which would also be available as a threefold medication to increase adherence, isn't in this circumstance. (Bateman et al.,2012)
The treatment of late motor complications of PD-
Typically, individuals without PD suffer changes in muscle control after several years of steady, persistent response to levodopa medication, with both the impact of a particular levodopa dosage growing increasingly less (wearing-off phenomenon). Mostly in mature instances, episodes of immobility unconnected to levodopa delivery happen (on-off phenomena). (Harding and Halliday.,12th may 2022) Upwards of half of patients will acquire motor oscillations and involuntary movements within 5 - 10 min after starting levodopa, including 20-30 cent developing dyskinesias during the first two years. The scenario is worse than in younger folks, with nearly all population is > the age of 40 suffering motor difficulties six weeks after joining levodopa. (Chamard et al.,2020) Decreasing the regular dose alone commonly causes individuals to become stiff and inflexible. When plasma levodopa levels rise or fall, biphasic dyskinesias can develop. They usually have a bigger impact on the less extremities. This was revealed by coincidence to get other qualities, notably performance in Parkinson's disease. There still is indication that drug can lessen the incidence of motor problems such as stiffness, 'off' spells, and dyskinesias. There is a somewhat high prevalence of adverse effects, which would include disorientation, hallucinations, ankle edema, and livedo reticularis, especially among the elderly. (Bateman et al.,2012)
Best Treatment of Alzheimer’s Disease available in market
As such there is no promising cure for Alzheimer till date, however many researches and trials are going on.
Cholinesterase inhibitors. By preserving a chemical messenger that Alzheimer's disease has diminished in the brain, these drugs promote cell-to-cell interaction. Most patients only have very slight clinical alleviation while using these medications, which are typically the first ones administered. Cholinesterase inhibitors are frequently used to treat neuropsychiatric patients' agitation and sadness. Donepezil, galantamine, and rivastigmine are some of the most often prescribed cholinesterase inhibitors.
Memantine (Namenda)- This medicine reduces symptoms of moderate to severe Alzheimer's disease by affecting brain cell communication network. It's frequently used in conjunction with a cholinesterase inhibitor. (Carrillo and Vellas.,2003)
Aducanumab (Aduhelm) - FDA just authorized aducanumab (Aduhelm) for the treatment of a few patients of Alzheimer's disease in June 2021. This is the first medicine licensed by the US Food and Drug Administration to treat Alzheimer's disease by identifying and eliminating amyloid plaques in the brain (Gorno-Tempini et al.,2019).
legal framework & legal basis for Parkinson
These notes are intended to provide guidance for the evaluation of drugs in the treatment of Parkinson’s disease. They follow the Directive 2001/83/EC, as amended and current and future EC and ICH guidelines, especially those on:
- Studies in support of special populations: geriatrics (ICH E7);
- The extent of population exposure to assess clinical safety for drugs intended for long-term treatment in non-life-threatening conditions (ICH El);
- General considerations for clinical trials (ICH-E8);
- Guideline on Clinical Trials in Small Populations;
- Statistical principles for clinical trials (ICH-E9);
- Choice of Control Group in Clinical Trials (ICH E10);
- Note for Guidance on the Investigation of Drug Interactions;
- Pharmacokinetic studies in man;
- Clinical testing of prolonged action forms, with special reference to extended-release forms;
- Dose response information to support product authorization (ICH E4);
- Guideline on medicinal products for the treatment of Alzheimer’s disease and other dementias (CPMP/EWP/553/95, Rev. 1). They are intended to assist applicants in the interpretation with respect to specific problems presented by products in PD.
Legal framework and legal basis for Alzheimer
This note follow general principles (4) and part of the Annex I to Directive 2001/83/EC as amended and relevant CHMP Guidelines, among them:
- Dose-Response information to Support Drug Registration (CPMP/ICH/378/95 (ICH E4))
- Statistical Principles for Clinical Trials (CPMP/ICH/363/96 (ICH E9)) - Choice of Control
Group in Clinical Trials (CPMP/ICH/364/96 (ICH E10))
- Guideline on adjustment for baseline covariates in clinical (EMA/CHMP/295050/2013)
- Guideline on Missing Data in Confirmatory Clinical Trials (EMA/CPMP/EWP/1776/99 Rev. 1)
- Points to Consider on Multiplicity Issues in Clinical Trials (CPMP/EWP/908/99)
- Guideline on the choice of a Non-Inferiority Margin (CPMP/EWP/2158/99)
- Extent of Population Exposure to Assess Clinical Safety (CPMP/ICH/375/95 (ICH E1A))
- Studies in support of special populations: geriatrics (CPMP/ICH/379/99 (ICH E7))
- Guideline on Clinical Trials in Small Populations (CHMP/EWP/83561/2005)
- Pharmacokinetic studies in man (EudraLex vol. 3C C3A)
- Guideline on the Investigation of Drug Interactions (CPMP/EWP/560/95/Rev. 1 Corr. 2**)
- Guideline on clinical evaluation of new vaccines (CHMP/VWP/164653/2005) Special consideration should be given to the qualification procedures as such and particularly for Alzheimer’s disease
(European Medicines Agency,2021b)
Before accepting a New Drug Application (NDA), the FDA and EMA ensure that it is of acceptable quality. When assessing a drug's effectiveness, the US FDA and EMA use similar factors. Typically, drug designations for Parkinson's and Alzheimer's disease are published on a monthly basis. (Thomas et al.,2021) The cumulative posts include the sponsor's name and address, the generic and commercial names of the drug, the date the medicine was designated, and the drug's usage. Because these ailments are commonly disregarded, such limits are advantageous to the development of such treatments and give sponsors with sufficient backing to get market authorization (Code of Federal Regulations,2013).
CHAPTER C - RESEARCH METHODOLOGY
The purpose of this research is to investigate the regulatory framework for two prevalent diseases, Parkinson's and Alzheimer's, for which there is no potential therapy. Both the European Medicines Agency and the US Food and Drug Administration have worked with several sponsoring corporations to establish a particular committee and legislative framework, but no results have been obtained too far. Comparative research on such medication laws for illnesses in Europe and the United States will be carried out, resulting in a tool for quantitative determination. The information will be displayed in the form of a chart or graphical literature.
'EUDRAVIGILANCE, FDA adverse event reporting system (FAERS)' is a critical resource for gathering information on both illnesses and improving treatment for populations suffering from Parkinson's and Alzheimer's disease. All major pharmacovigilance agencies are in continual contact with the World Health Organization, which has expanded its network to encompass nearly all countries in Europe and throughout the world. They offer a variety of services, including mapping of rare disorders utilizing databases like UMLs, MedDRA, GARD, OMIM, and ICD 10.
In addition, a case study will be demonstrated on an authorized drug used for treatment of Parkinson and Alzheimer. Basically, the biological activity of authorized drugs to see multiple metabolic pathways and cellular processes and why cure is still not possible with these drugs.
The research also aims at analyzing the challenges which is faced during the legal work and clinical trials for both Alzheimer and Parkinson disease. And why most of the sponsoring companies don’t put money and time on such drugs and research even after getting different investments like from US government or WHO. With this getting why different approach is taken for such disease as legal work in both European Medical Agency and US Food Drug Administration.
To explore the market authorization process for which the treatment is approved. And compare procedure of US regulatory framework with European Framework with help of case study
REFRENCING
European Medicines Agency (2021a). Orphan designation: Overview - European Medicines Agency [online]. Available from:
https://www.ema.europa.eu/en/humanregulatory/overview/orphan-designation-overview [Accessed 01 November 2022].
Medunik USA. (2021). Rare Diseases & Orphan Drugs [online]. Available from: https://medunikusa.com/rare-diseases-and-orphan-drugs [Accessed 31 october 2022].
European Medicines Agency (2021b). Legal framework: orphan designation - European Medicines Agency [online]. Available from: https://www.ema.europa.eu/en/human- 14 regulatory/overview/orphan-designation/legal-framework-orphan-designation#review- oforphan-regulation-section [Accessed 8 November 2022]
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Albin, R.L. and Frey, K.A., (2003). Initial agonist treatment of Parkinson disease: a critique. Neurology, 60 (3), pp.390-394.
Bohnen, N.I., Kaufer, D.I., Ivanco, L.S., Lopresti, B., Koeppe, R.A., Davis, J.G., Mathis, C.A., Moore, R.Y. and DeKosky, S.T., 2003. Cortical cholinergic function is more severely affected in parkinsonian dementia than in Alzheimer disease: an in vivo positron emission tomographic study. Archives of neurology, 60 (12), pp.1745-1748.
Braak, H., Del Tredici, K., Rub, U., De Vos, R.A., Steur, E.N.J. and Braak, E., 2003. Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiology of aging, 24 (2), pp.197-211.
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Frequently Asked Questions
What is the primary focus of the provided document?
The document is a language preview from a publishing company, containing OCR data intended for academic use. It primarily focuses on analyzing themes related to Alzheimer's and Parkinson's disease, including potential treatments, legal frameworks, and research methodologies.
What are the main chapters covered in the language preview?
The document includes an introduction (Chapter A), a literature review (Chapter B), and a section on research methodology (Chapter C). It also contains a table of contents and a list of references.
What topics are discussed in the Literature Review chapter (Chapter B)?
Chapter B covers topics such as understanding Parkinson's and Alzheimer's diseases and the challenges in treating them, available treatments for both diseases, and the legal frameworks and legal basis relevant to each condition.
What information is provided regarding treatments for Parkinson's disease?
The document discusses various treatments for Parkinson's disease, including first-line levodopa treatment, dopamine agonist treatment, MAO-B inhibitors, and COMT inhibitors. It also touches on the treatment of late motor complications of Parkinson's disease.
What information is provided regarding treatments for Alzheimer's disease?
The document mentions that there is no promising cure for Alzheimer's to date, but discusses treatments like cholinesterase inhibitors, Memantine (Namenda), and Aducanumab (Aduhelm). It also describes that FDA has approved aducanumab (Aduhelm) for the treatment of patients of Alzheimer's disease by identifying and eliminating amyloid plaques in the brain.
What is mentioned about the legal frameworks for Parkinson's and Alzheimer's?
The language preview provides notes and guidelines intended for the evaluation of drugs in the treatment of Parkinson’s and Alzheimer’s disease. It follows legal directives and ICH guidelines.
What research methodology is outlined in Chapter C?
Chapter C details the research approach, including investigating the regulatory frameworks for Parkinson's and Alzheimer's diseases in the European Medicines Agency and the US Food and Drug Administration. It also mentions the use of databases like EUDRAVIGILANCE and FDA adverse event reporting system (FAERS) for gathering information. A case study about authorized drugs is mentioned.
What is EUDRAVIGILANCE, and how is it related to this research?
EUDRAVIGILANCE is a critical resource for gathering information on Parkinson's and Alzheimer's diseases and improving treatment for populations suffering from these illnesses. It's a pharmacovigilance agency connected with the World Health Organization.
What challenges are identified in researching and treating Alzheimer's and Parkinson's diseases?
The document highlights challenges such as the complexity of brain activity, the need for unique patient therapies, the lack of comprehensive safety and risk data, and the absence of known cures. It also mentions difficulties in the legal work and clinical trials and potential hesitations from sponsoring companies to invest in such research.
What is the ultimate goal of the research outlined in this language preview?
The research aims to investigate and compare medication laws for Alzheimer's and Parkinson's diseases in Europe and the United States. It seeks to understand the challenges in the legal work and clinical trials for these diseases and the market authorization process for approved treatments.
- Quote paper
- Kunal Kunal (Author), 2022, Complications and Safety Monitoring in Parkinson's and Alzheimer's Disease. Why Treating These Diseases is Challenging, Munich, GRIN Verlag, https://www.grin.com/document/1497163
