This is a short post about this publication with an interesting title.

I thought it was about the acute anxiety of carers when their loved one could not eat anymore, actually, it is about how doctors in British hospitals manage patients who could not take their medication orally.

The alternatives are either a soluble medication, a topical patch, or a nasogastric tube.

I wonder if there is not a more urgent problem for patients that could not swallow, than taking their medication.

I am pleased that two new articles bear a similar message: That neurodegenerative diseases can't be understood with the paradigm acquired with communicable diseases.

This paradigm tells us that as the pathogen is quite homogeneous, so is the disease phenotype. This is indeed wrong for non-communicable diseases like cancers and is even wrong for some communicable diseases like COVID-19 where the pathogens have heavily mutated.

One of these articles is "Serena Verdi et al, Personalizing progressive changes to brain structure in Alzheimer's disease using normative modeling".

The authors looked at 3233 brain scans. The number of non-standard brain structures increased over time in people with Alzheimer's disease. Patterns of change in outliers varied markedly between individual patients with Alzheimer's disease.

The authors say: "I think we need to pivot towards a new way of thinking to get away from the idea that this (brain) area is important, this area isn't". The big picture and the individual variability contained within it, is what counts.". Some of this individual variability may stem from the fact that many people with Alzheimer's have more than one cause of cognitive illness.

This idea that "we need to pivot towards a new way of thinking to get away from the idea that this (brain) area is important, this area isn't" is certainly important when we think of other neurodegenerative diseases such as ALS or Parkinson's disease.

Our knowledge about Parkinson's disease is limited. The official narrative is that Parkinson's disease is characterized by progressively expanding nerve cell death originating in substantia nigra, a midbrain region that supplies dopamine to the basal ganglia, a system involved in voluntary motor control. The cause of this cell death is poorly understood but involves alpha-synuclein aggregation into Lewy bodies within the neurons. Substantia nigra is really a tiny part of the brain, and other studies have already revealed a wider involvement in the brain. I guess we would make significant progresses in the disease knowledge if we acknowledge that if alpha-synuclein is involved in Parkinson's disease, it is unlikely its effects are limited to a tiny portion of the brain, as alpha-synuclein is abundant in the brain, while smaller amounts are found in the heart, muscle and other tissues and Lewy bodies are in the midbrain and the cortex.

Another interesting article is: "Ophthalmate is a new regulator of motor functions via CaSR: implications for movement disorders".

While the official narrative is that Parkinson's disease is characterized by neuronal death in substantia nigra, which supplies dopamine to the basal ganglia, a system involved in voluntary motor control, it has been known for decades that robust motor activity can happen in Parkinson's mouse models when L-DOPA conversion to dopamine is blocked! The motor improvement is larger than in the conventional case where L-DOPA is metabolized in dopamine. The authors hypothesized that there was an alternative pathway or mechanism, independent of dopamine signaling.

The authors sought to determine the metabolites associated with the pronounced hyperactivity observed. They observed that the peak in motor activity induced by inhibiting L-DOPA conversion into dopamine in Parkinson’s disease mice was associated with a surge (20-fold) in brain levels of the tripeptide ophthalmic acid (also known as ophthalmate in its anionic form). When they administered ophthalmate directly into mice's brains, it rescued motor deficit in a dose-dependent manner.

The team investigated the molecular mechanisms underlying ophthalmate’s action and discovered, that ophthalmate binds to and activates the calcium-sensing receptor (CaSR). To strengthen their findings, they verified that a CaSR antagonist inhibits the motor-enhancing effects of ophthalmate.

A link between Parkinson's disease and the calcium-Sensing Receptor is interesting as CaSR also Mediates β-Amyloid production. There is only one other publication that explicitly links the disease to CaSR. Calcium acts in a number of signal transduction pathways as second messengers, so maybe it is not wise to read too much about a link between Parkinson's disease and CaSR, but finding that lack of dopamine is not the main cause of Parkinson's disease, is a major finding.

As loving standards progressed during the last century, the diet became richer, and health conditions, such as gout, which were usually associated with people with high living standards became increasingly more common. It was soon recognized that acid uric imbalance was associated, not only with gout, but with a range of diseases. Most striking associations are inverse correlations as they should teach us something. One such inverse correlation is between elevated acid uric levels and Parkinson's disease. On the contrary, there is an association between low levels of acid uric and patients with Parkinson's disease, or multiple sclerosis. Yet something related to Parkinson's disease may cause low uric acid (reverse causation). Indeed, Parkinson’s disease is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and the presence of Lewy bodies and Lewy neurites, which mainly consist of aggregates of α-synuclein. It is believed that α-synuclein aggregates poison the brain's cells and indeed especially this tiny part of the brain named "substantia nigra". Yet like other protein aggregates, they may form to protect the brain against some external aggression or stressing event. So the biological mechanisms underlying α-synuclein relationships with dopaminergic neurons have never been firmly established.

While the most frequently proposed mechanism for uric acid's inverse association with Parkinson's disease is that it is an antioxidant, however, clinical trials aiming to raise uric acid levels failed to slow the progression of Parkinson's disease. Then some scientists argued that many studies have pointed to mitochondrial dysfunction in Parkinson's disease. One of the major functions of mitochondria is producing energy in the form of ATP, which is quantitatively the most abundant of all purines in the body. As serum uric acid is a by-product of purine metabolism, mitochondrial dysfunction, and energy failure in Parkinson's disease may lead to low serum uric acid levels. An excellent review can be found here.

There is ample evidence that neurons can internalize extracellular aggregates by endocytosis. Some studies have shown that acid uric inhibits α-syn endocytosis by neurons thereby limiting the progression of the disease.

To precise the relation between Parkinson's disease and uric acid, a study shows that factors other than the purine metabolic system might influence CSF values of uric acid and that purine recycling pathways may be impaired. enter link description here

The current study found a significant reduction in hypoxanthine and inosine levels in the CSF of patients with PD but not in the serum. This small study, published in Nature Parkinson's Disease Journal, was published in preprints last year. Basically, it confirms previous findings such as those reported in the 2023 review above.

A new study explores the evolving therapeutic landscape for Parkinson's disease (PD), emphasizing the growing interest in complementary therapies, particularly dance. While it's specific to one culture, I think we could use it in any culture, as long as physical therapy is done in a pleasant social setting. Here the authors report that the enjoyment factor associated with Garba dance likely contributed to better adherence to the treatment. Patients reported having fun, which is crucial for long-term engagement with any form of physical therapy.

Overview of Parkinson's Disease Treatment The primary treatment for Parkinson's disease is dopamine replacement therapy, which targets motor symptoms. However, as the disease progresses, the effectiveness of these medications diminishes, and patients often experience more pronounced nonmotor symptoms, including cognitive decline, mood disorders, and sleep disturbances. These nonmotor symptoms are particularly resistant to pharmacological treatments and negatively impact quality of life. In addition, dopamine replacement therapies create new mental (hallucinations) and physical challenges (cardiac fibrosis).

To address these challenges, a multidisciplinary approach involving surgery, physical therapy, occupational therapy, and cognitive interventions is often necessary. Yet, adherence to such therapies can be challenging, particularly among older adults.

Complementary Therapies for Parkinson's Disease Various complementary activities like dance, music, theatre, art, and Tai Chi have been studied as potential therapeutic options in recent years. Though evidence supporting these therapies is still in its early stages, initial findings suggest that they may positively affect nonmotor symptoms, psychological well-being, and overall quality of life. For example, music therapy has been reported to benefit motor and nonmotor symptoms, cognition, and emotional health. Similarly, active theatre therapy may help patients develop social and emotional skills in a supportive environment, potentially reducing depression and social stigma. Tai Chi has shown promise in improving balance and reducing the frequency of falls in patients.

Dance Therapy in Parkinson's Disease Among complementary therapies, dance has garnered significant attention for its potential to manage both motor and nonmotor symptoms of Parkinson's disease. Studies suggest that dance may enhance cognitive function, improve motor skills, and even increase dopamine release in the brain. Furthermore, the enjoyment and social aspects of dance make it an appealing form of physical activity, potentially enhancing treatment adherence. Various dance forms, including Irish set dancing, Argentine tango, and ballroom dances like the Waltz and Foxtrot, have been shown to improve balance, gait, and locomotion in Parkinson's patients, particularly in Western contexts. In India, traditional dances like Bharatnatyam and Kathak have been explored for their therapeutic potential, although their complexity makes them less accessible to all patients.

Pilot Study: Garba Dance as a Therapy for Parkinson's Disease The pilot study evaluated Garba, a popular Indian dance form, as a therapeutic intervention for Parkinson's disease. Garba involves relatively simple movements, making it more accessible than other Indian dance forms. The study assessed the effects of Garba dance on motor and nonmotor symptoms, cognitive functions, and mood. The results were promising, particularly in terms of improvements in motor symptoms, as measured by the Unified Parkinson's Disease Rating Scale (UPDRS). To say it in a few words, symptoms went from severe to moderate in 12 weeks. There were three groups, one practicing Garba dance, the other physical therapy, and the last one was the control. All groups took their medications. Obviously, it was not possible to make a fully blinded test where patients ignore which drug they are administrated. Still, UPDRS raters were blinded to treatment allocations at all time points in the study.

The UPDRS encompasses different aspects of the disease, it ranges from 0 to 260 but a value below 30 usually means a mild disease. All patients had a score of 35 at the beginning of the study, indeed severely disabled patients would not be able to participate in this study.

Motor Symptom Improvement: Patients in the Garba dance group experienced significant improvements in UPDRS scores after 12 weeks (going from ~35 to ~20), surpassing those in the physical therapy and control groups. The physical therapy group went from ~36 to ~30, while the situation worsened for the control group (~35 to ~37).

Mood and Sleep Benefits: Although the study found no significant improvement in nonmotor symptoms like activities of daily living (ADL) or cognition, it did observe improvements in mood and sleep. This is consistent with other studies that have linked dance therapy to enhanced emotional well-being and reduced depressive symptoms in Parkinson’s patients.

Limitations of the Study While the study results are encouraging, the authors acknowledge several limitations. The small sample size and short duration of the study prevent definitive conclusions. Additionally, there was no follow-up after the study to assess the persistence of the observed effects. The study also did not capture differences in motor symptoms during the "on" and "off" medication states, which could have provided more nuanced insights. Another concern was the incidence of near falls, though no actual falls were reported, likely due to the close monitoring of participants.

Implications for Future Research and Practice Despite its limitations, this pilot study suggests that Garba dance may be a viable complementary therapy for Parkinson's disease, particularly for patients with a cultural affinity for dance. The noticeable improvements in motor symptoms, mood, and sleep warrant further investigation in larger, more rigorous trials. The study supports the idea that enjoyable, culturally relevant therapies can enhance treatment adherence and improve the quality of life for Parkinson’s patients.

In conclusion, while Garba dance should not replace traditional physical therapies in India, it presents an additional option within a multidisciplinary treatment plan for managing mild-to-moderate Parkinson's disease.

After weeks after weeks of uninteresting publications in neurodegenerative diseases, two publications, at last, are a bit above the lot.

Plateaus in ALS

The first article is about genetic analysis of cases of ALS reversal, or maybe it's not reversals but long duration plateaus in the disease course. As usual with the use of "reversal" word, Dr. Bedlack is involved.

He and his team found that in approximately 1% of patients, there is a plateau phase where the disease stops progressing for a long time. Studying those patients might teach new information. Bedlack and colleagues think they found that those patients have a different genetic code in areas related to insulin growth factor (IGF-1).

IGF-1 was tested in ALS a long time ago, and some interesting results were obtained. It was at a time were the criteria to judge if a clinical trial succeeded were much more stringent than today. Maybe it would be interesting to revisit these trials.

there is also the possibility that an IGF-1 therapy works with 1% of patients, but not with other patients.

Mitigating hydroxyl radicals and excess iron in Parkinson's disease

The other article is about the role of Iron in Parkinson's disease. Its writing style is not academic, yet the authors claim they were able to improve the state of disease in three Parkinson's patients by making them inhale (for one and a half hours!) a gas mixture containing hydrogen. They say hydrogen could dissolve in blood, reach the brain (it is a tiny molecule), and chelate unmetabolized iron.

The authors explain that when there are too many iron ions in the brain for ferritin to mitigate its oxidative effect, the iron ions are released into brain cells and mitochondria. Hydroxyl radicals (HO) with strong oxidizing power are produced, resulting in cellular and mitochondrial damage. In the views of the authors, hydrogen reacts with hydroxyl radicals resulting in water, so the toxicity of hydroxyl radicals is mitigated.

Yet it's not clear to me, why iron ion deposition results in hydroxyl radicals and what happens to iron after hydrogen reacts with hydroxyl radicals.

Iron toxicity in neurodegenerative diseases and aging has been suspected for a long time, yet all chelating drugs that were tried were unable to significantly change the course of the disease.

Some people advocate for Parkinson's patients to consume mannitol. Many individuals affected by the disease began consuming daily oral mannitol. Self-reported outcomes included an improved sense of smell, a reduction in the dose of PD medications, and general improvement in well-being. A clinical trial was done at Hadassah Medical Center in Israel by David Arkadir and colleagues.

The lobby group CliniCrowd was probably instrumental in this decision.

The study lasted 36 weeks and included four dose escalations of oral mannitol (manufacturer Roquette, France) or dextrose as a placebo from 2.5 g to a maximal dose of 18 g per day. The COVID-19 pandemic in 2020 dramatically slowed the recruitment rate in the 3rd year of the clinical trial and led to the decision to earlier trial termination. They did not observe a clear reduction in Parkinson's symptoms. It is possible that a longer exposure would enable clinically to demonstrate disease modification. Anyway, such a high dose of mannitol is not without innuendoes, mannitol is hypertonic, it forces water to be excreted from cells. Yet the mechanism by which mannitol reduces α-synuclein accumulation in PD models was still unknown.

In 2022 another study showed that glycation agents (sugars) can ameliorate α-synuclein folding. Glycation is increased in the brains of hyperglycemic patients. Alpha-synuclein (αSN), a central player in the etiology of Parkinson’s disease, can be glycated so reducing αSN fibril formation. The best glycating agents were unfortunately toxic, but one agent was mildly efficacious while not toxic: Mannose.

Mannitol, while usually derived from fructose, can also be derived from a mannose by reduction. In the human body, mannose residues are used to assemble N-glycans by adding them to a dolichol phosphate (Dol-P) core in the Endoplasmic Reticulum (ER) of cells.

There's a growing body of research suggesting a connection between abnormal N-glycans and neurodegenerative diseases like Alzheimer's and Parkinson's. N-glycans are sugar chains attached to proteins in a specific way, and changes in their structure or abundance seem to play a role in these diseases. This means the sugar chains are either attached differently, have different structures, or are present in abnormal amounts.

N-glycans can influence how proteins fold, interact with other molecules, and get transported within cells. In a recent publication, scientists analyzed neurons in iPSC midbrain cultures derived from patients with Parkinson's disease and they discovered the disruption of a metabolic pathway, the hexosamine pathway. The hexosamine pathway is important for protein synthesis, transport, and folding in the neuron's endoplasmic reticulum. The hexosamine pathway produces N-linked glycans, essential molecules that support protein folding in the endoplasmic reticulum.

The hexosamine pathway (a biological pathway is the way a molecule is created from components) uses glucose and uridine-5’-triphosphate to generate N-linked glycans for protein folding in the endoplasmic reticulum. In Parkinson's midbrain cultures, however, this N-glycosylation process was interrupted, causing protein misfolding and accumulation of α-synuclein.

Accelerating glucose flux through the hexosamine pathway rescued hydrolase function and reduced pathological α-synuclein.

So as a non-scientist, I can conclude this post by saying that there is some rationality in using mannitol in Parkinson's disease, while it might not be the silver bullet people are waiting for.

In February, a proposal was made to diagnose Parkinson's disease based on the presence of α-synuclein accumulation, even in the absence of specific clinical symptoms. This proposal follows a similar trend observed in other neurodegenerative diseases. Clinically, this approach is somewhat controversial as it would label asymptomatic individuals as diseased. Furthermore, it raises questions about why individuals in good health would seek medical consultation.

This follows a similar trend in other neurodegenerative diseases. This initiative may be driven by the pharmaceutical industry's frustration over unsuccessful clinical trials. By using molecular criteria, clinical trials could achieve higher success rates, despite the persistence of clinical symptoms. This strategy is already evident in the Alzheimer's field, where several drugs have been approved without significantly alleviating symptoms.

This reflects a situation with disease animal models which are successfully cured by many proposed therapies but when those therapies are applied to humans they fail.

The proposal has not been universally welcomed but is likely to gain approval from regulatory bodies due to pressure from patient associations and the pharmaceutical industry to demonstrate progress.

Here is a small list of readers' reactions and answers by authors:

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00211-4/fulltext

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00212-6/fulltext

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00213-8/fulltext

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00214-X/fulltext

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00215-1/fulltext

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00217-5/fulltext

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00222-9/fulltext

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00225-4/fulltext

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(24)00233-3/fulltext

From a political and economic perspective, this approach is problematic. It would lead to the treatment of healthy individuals in an already overburdened healthcare system. Additionally, these treatments are expected to be very costly while being ineffective on clinical symptoms.

We went too far into a mechanical and technological vision of medicine led by molecular biology.

Nous sommes dans une période creuse de résultats scientifiques qui durera sans doute tout l'été, aussi voici un résumé d'un article passionnant racontant comment un médecin et chercheur Turque, Sibel Özekmekçi, a développé la maladie de Parkinson, et comment elle a géré cette maladie. L'article qui est consultable à cette adresse a été résumé, traduit et simplifié pour les besoins du format de publication sur PadiracInnovation. En tant que neurologue expérimenté spécialisé dans la maladie de Parkinson (MP) et d’autres troubles du mouvement, l'auteur raconte comment elle a diagnostiqué sa propre maladie de Parkinson, qui a commencé par des symptômes très légers. Dans cet article, elle a choisi de documenter ses observations et ses expériences au cours de ce voyage, en fournissant des informations du point de vue à la fois du patient et du spécialiste.

À travers cet article de synthèse, son objectif était de fournir un compte rendu concis de son parcours scolaire, de son implication professionnelle dans le domaine de la maladie de Parkinson, des premiers symptômes et de la progression de la maladie, des symptômes moteurs et non moteurs associés à la maladie de Parkinson, ainsi que l'impact psychologique de la maladie lors des étapes de reconnaissance, d'acceptation et d'intériorisation.

Après ses études de médecine à la Faculté de médecine d'Istanbul, Sibel Özekmekçi est devenu professeur agrégé et, avec le médecin spécialiste Güneş Kiziltan, ils ont créé le « Groupe de la maladie de Parkinson et des troubles du mouvement » et ont commencé à consulter des patients dans une clinique externe privée.

Dans les années suivantes, ils ont collaboré avec des neurologues et des physiothérapeutes de la Faculté de médecine d'Istanbul de l'Université d'Istanbul pour transmettre les connaissances médicales actuelles sur la maladie de Parkinson aux patients et aux membres de leur famille. Ainsi l'auteur a souvent soigné des patients atteints de la maladie de Parkinson et occasionnellement des patients souffrant de troubles du mouvement.

A partir de l'âge de 70 ans des contractions involontaires peu nombreuses sont apparus dans le pouce de sa main droite, et même si elle soupçonnait que certaines d'entre elles pourraient signifier un début de maladie de Parkinson, elle a hésité à se diagnostiquer, car les contractions étaient sporadiques. Elle ne s'y était pas attardée à l'époque, mais en regardant ses photographies prises à cette époque, après le diagnostic, maintenant elle distingue bien la présence d'une légère chute des lèvres du coté droite, ce qui est fréquent chez les patients présentant une maladie de Parkinson. Puis au fil des ans, des douleurs sont apparues dans la région fémorale antérieure de sa jambe droite lors de longues marches. Elle a aussi fait une chute bénigne en bord de mer, mais sans comprendre la raison de cette chute. C'est aussi à cette époque qu'elle a remarqué qu'elle se penchait beaucoup en avant lorsqu'elle se promenait et que sa légère bosse, qui était là depuis l'enfance, avait augmenté de taille. Un jour, alors qu'elle a commencé à avoir des tremblements constants au repos dans le pouce de sa main droite, elle a alors réalisé que le problème était grave. Le tremblement se présentait sous la forme d'une flexion et d'une extension du doigt, mais elle ne voulait pas encore accepter le diagnostic Quelques jours plus tard, elle a également eu un tremblement au repos dans l'index de la main gauche, mais cela ne s'est pas reproduit. De nombreux patients ne consultent pas un médecin à ce stade mais seulement lorsque la maladie progresse et que les symptômes s'accentuent. Elle a alors consulté un collègue spécialiste de cette maladie.

Aux premiers stades, avant l'âge d'environ 60 à 65 ans, des agonistes dopaminergiques sont prescrits tels que le piribédil en deux à trois doses quotidiennes, le pramipexole à action prolongée en dose unique ou des inhibiteurs de la monoamino oxydase-B tels que la rasagiline en dose unique sont recommandés. Chez les personnes âgées et chez les patients de tout âge à un stade avancé de la maladie, la lévodopa, est le médicament le plus couramment administré. Bien qu'âgée alors de 72 ans, elle a cependant préféré se faire prescrire les médicaments adjuvants en raison de la nature légère de ses symptômes et de leur facilité d'utilisation.

Elle n’a pu expliquer le diagnostic à sa fille qu’une vingtaine de jours plus tard, "pour ne pas la bousculer". Sa fille a été très surprise et, bien sûr, très bouleversée par l'ironie du destin, car Sibel Özekmekçi était médecin et exerçait depuis de nombreuses années dans ce domaine. Au cours de sa dernière année et demie d'exercice professionel, elle n'a jamais parlé de sa maladie à ses collègues.

À cette époque, elle a également partagé le diagnostic avec son cher ami psychiatre, le Prof. Şahika Yüksel. Son psychiatre, l'a encouragé à s'ouvrir à ses proches de son état. Ainsi, un an et demi après le diagnostic, elle a commencé à révéler occasionnellement qu'elle était atteinte de la maladie de Parkinson. En effet, en partageant le diagnostic avec d’autres, elle avait l’impression que son fardeau s'allégeait. Elle a alors compris qu’il valait mieux accepter l’apparition des symptômes moteurs.

C'était aussi une relative consolation pour elle de savoir que sa maladie ne faisait pas partie des syndromes « Parkinson plus » dont l'évolution rapide rend les patients handicapés en peu de temps. Les quelques amis qui connaissaient sa maladie et sa fille lui ont conseillé de faire un suivi auprès d'un autre médecin expérimenté. Celui-ci a légèrement augmenté la dose de lévodopa/bensérazide. Pour l'hypersalivation, il a suggéré un collyre au maléate de timolol appliqué sur la langue, qui peut être efficace chez la plupart des patients, mais malheureusement, cela n'a eu aucun effet sur elle. Cependant, des contractions involontaires des fléchisseurs semblables à une dystonie ont commencé au niveau des deuxième et troisième orteils de son pied droit, particulièrement persistantes l'après-midi et le soir. Elle a considéré ces contractions comme une dyskinésie induite par la lévodopa, et elle a commencé à prendre un comprimé d'amantadine.

On sait que les patients atteints de la maladie de Parkinson peuvent présenter de nombreux symptômes non moteurs en plus des symptômes moteurs. Cependant, sans symptômes moteurs, le diagnostic clinique de la maladie est peu probable chez les patients présentant uniquement ces problèmes. Après confirmation du diagnostic elle a pensé que son insomnie, qui durait depuis 20 ans, pourrait être une manifestation présymptomatique et non motrice de la maladie.

Les symptômes qu'elle a personnellement remarqués chez elle, mais qu'elle a seulement reconnu qu'il s'agissait de signes non moteurs de la maladie après avoir posé le diagnostic sont les suivants : - Un sentiment de froid - Beaucoup d’anxiété et de stress extrême. - Elle a du mal à expliquer ses efforts pour cacher le diagnostic à l'époque ; peut-être ne voulais-elle pas susciter la pitié ou attirer l'attention des autres.

Aujourd'hui, sa maladie est bien contrôlée grâce aux médicaments à la dopamine. Bien qu’il n’existe actuellement aucun médicament permettant de ralentir la progression de la maladie de Parkinson, il existe des médicaments qui procurent un soulagement symptomatique. Cependant, même si elle est d’accord avec les récentes observations scientifiques qui montrent que l’exercice ralentit la progression de la maladie, elle doit admettre qu'elle néglige d’en faire régulièrement. Aujourd’hui, parfois, surtout lorsque elle tient un objet lourd, elle éprouve un léger tremblement dans les deux mains. Elle a du mal à se relever après être resté assise longtemps, alors elle préfère se lever souvent et marcher pour surmonter ce problème.

En se qui concerne son futur Sibel Özekmekçi sait que dans la maladie de Parkinson, la diminution partielle de la sérotonine et de la noradrénaline dans le cerveau peut conduire à l’émergence d’une dépression chez de nombreux patients. Il a aussi été souligné la présence de diabète de type II chez les patients atteints pourrait constituer un facteur de risque « prodromique » dans le développement de la maladie.

De même, il a été constaté que l'hypothyroïdie et l'utilisation à long terme de lévothyroxine pouvaient également constituer un risque, et la prévalence de cette maladie s'est avérée élevée chez les patients souffrant d'hyperthyroïdie ainsi que hypothyroïdie. L'auteur doit constamment suivre ses heures de prise de médicaments au cours de la journée et organiser sa vie quotidienne en fonction des intervalles pendant lesquels elle peux manger.