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Thursday, April 25, 2024
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Latest Developments In Parkinson’s Treatment

What Is Fetal Cell Transplantation

New Advances Make DBS Therapy More Effective For Treating Parkinson’s Disease

Fetal cell transplantation is a procedure in which fetal cells are implanted into the brains of people with Parkinson’s disease to replace the dopamine-producing cells in the substantia nigra. Although promising, this area of research is one of the most controversial. Some studies have found that fetal cell transplantation caused an increase in severe involuntary movements due to too much dopamine in the brain. There are also moral and ethical objections to the use of fetal cell implants. As a result, other methods of treatment are being explored.

The Parkinsons Disease Medication Pipeline

The pipeline for Parkinsons disease medications is extremely crowded these days, with multiple medications at various stages of research development. This is very exciting news for the PD community and is a perfect example of the hope in progress part of our organizations motto. It is thrilling to see the research that is underway, especially the potential treatments that have already made it to the clinical trial phase of development. However, this progress brings with it the welcome challenge of keeping track of all the potential compounds that are in research development! Recently, a review was published in the Journal of Parkinsons Disease which cataloged the 145 compounds that are currently being studied in humans via clinical trials for PD. This is a staggering number and is even more exceptional when you consider the many more compounds that are not quite yet ready for human trials, but are currently being studied in the laboratory in test tubes, cell culture or animal models of PD. The number also does not account for compounds that have been studied in small clinical trials, garnered promising data, and will be studied in larger clinical trials in the near future but are not being tested in clinical trials right now.

Some background on the review

New Medications For Off Time

A number of new medications approved recently are designed to reduce OFF time. These medications fall into two major categories:

  • Medications that lengthen the effect of a carbidopa/levodopa dose
  • Medications that are used as needed if medication effects wear off

Well give specific examples below. In general, new medications that extend the length of a carbidopa/levodopa dose are used if OFF time is somewhat predictable and occurs prior to next dose. New medications that are used as needed are most beneficial when OFF time is not predictable.

New medications that lengthen the effect of a dose of carbidopa/levodopa

  • Istradefylline is an adenosine A2A receptor antagonist which was approved in the US in 2019 as an add-on therapy to levodopa for treatment of OFF time in PD. Unlike many of the other medications, it has a novel mechanism of action and is the first medication in its class to be approved for PD. It acts on the adenosine receptor, which modulates the dopaminergic system, but is not directly dopaminergic. The drug was developed in Japan and underwent clinical trials both in Japan and in the US.
  • Opicapone is a catechol-O-methyltransferase inhibitor that is taken once a day. It was approved in the US in 2020 as an add-on therapy to levodopa for motor fluctuations.

New formulations of levodopa designed to be used as needed if medication effects wear off

Other medications used as needed if medication effects wear off

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Glucocerbrosidase Enhancing The Cells Lysosomal System

GBA is a gene that increases the risk of developing PD. The GBA protein works in the lysosome, the garbage disposal system of the cell, breaking down cellular products that can be harmful to the cell. Having two abnormal GBA genes causes Gauchers disease, which is characterized by the buildup of these cellular products. This results in fatigue, bone pain, easy bleeding and an enlarged spleen and liver. When a person inherits only one abnormal gene, he or she does not develop Gauchers disease however, they do incur a small increased risk of PD. Most people with one mutated GBA gene do not develop PD.

Enzyme replacement therapy, in which the GBA protein is given intravenously, is available as a treatment for Gauchers disease. This protein is too big to cross the blood-brain-barrier however, and so it does not enter the brain and does not treat any symptoms caused by the abnormal buildup of cellular components in the brain. The following strategies were developed in an attempt to compensate for the effects of the GBA mutation in the brain:

  • Ambroxol, approved in Europe for respiratory illnesses, improves the function of GBA in neurons NCT02941822 and NCT02914366
  • These small molecules can cross the blood-brain-barrier and help decrease the amount of accumulated cellular products in the brain:
  • A gene therapy trial of PR001A which introduces the un-mutated GBA gene into the brain is also underway NCT04127578
  • Scientists Believe Cancer Drug Candidate Could Treat Parkinsons

    Promising New Therapy For Parkinsons Disease  Southwest Florida

    Researchers have identified a way to block the action of a toxic protein believed to play a role in Parkinsons disease through an antibody that already is the subject of clinical trials targeting cancer and autoimmune disorders.

    LAG3 is a protein which in humans is encoded by the LAG3 gene that plays an important role in the immune system. Johns Hopkins University researchers discovered a previously unrecognized role for LAG3 which may have critical implications for understanding how -synuclein is connected to development of PD.

    The universitys Parkinsons study hinges on how abnormal clumps, or aggregates, of -synuclein enter brain cells by passing through transmembrane receptors, which act as a gate admitting only the correct proteins to enter brain cells. Researchers found that LAG3 has a heavy preference for latching onto -synuclein and plays a role in transporting them between cells.

    They followed up by studying how mice bred without the toxic protein and mice injected with the LAG3 antibodies reacted to -synuclein protein. They found that mice injected with LAG3 antibodies were almost completely protected from the Parkinsons-like symptoms that would typically result from -synuclein than control mice.

    If the trials targeting LAG3 antibodies prove them safe and effective then drugs already in the pipeline for cancer treatment could potentially benefit PD patients as well, researchers said.

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    The Latest Developments In Parkinsons Treatment: What Patients And Caregivers Need To Know

    Select Justice » Paraquat » The Latest Developments In Parkinsons Treatment: What Patients and Caregivers Need To Know

    Its devastating to watch a loved one live with Parkinsons disease. The progressive condition doesnt just affect the person with the diagnosis its also hard on caregivers, who are often forced to make difficult decisions on how to care for their loved one.

    Medications for Parkinsons can significantly help the motor issues associated with the disease. Current Parkinsons treatments only fight symptoms, however they do nothing to stop the progression of the disease, which is caused by a loss of neurons.

    Research on potential causes of and treatments for Parkinsons disease is ongoing. Recent research has shown a possible link between pesticide exposure and the development of Parkinsons disease, particularly in regards to the pesticide paraquat. Researchers are hopeful that new treatment protocols continue to effectively fight the symptoms of Parkinsons disease-related to pesticide exposure.

    Parkinsons disease research can be devastatingly slow. To speed treatment research, the Coalition Against Major Diseases has created a data-sharing partnership between non-profits, pharmaceutical companies, and government organizations to spearhead Parkinsons research in the most efficient way possible.

    Here, well explore the latest treatments for Parkinsons disease, as well as the treatment advancements that are likely to be made in the coming years.

    What Are The Symptoms Of The Disease

    The four primary symptoms of PD are:

    • Tremor. Tremor often begins in a hand, although sometimes a foot or the jaw is affected first. The tremor associated with PD has a characteristic rhythmic back-and-forth motion that may involve the thumb and forefinger and appear as a pill rolling. It is most obvious when the hand is at rest or when a person is under stress. This tremor usually disappears during sleep or improves with a purposeful, intended movement.
    • Rigidity. Rigidity , or a resistance to movement, affects most people with PD. The muscles remain constantly tense and contracted so that the person aches or feels stiff. The rigidity becomes obvious when another person tries to move the individuals arm, which will move only in ratchet-like or short, jerky movements known as cogwheel rigidity.
    • Bradykinesia. This slowing down of spontaneous and automatic movement is particularly frustrating because it may make simple tasks difficult. The person cannot rapidly perform routine movements. Activities once performed quickly and easilysuch as washing or dressingmay take much longer. There is often a decrease in facial expressions.
    • Postural instability. Impaired balance and changes in posture can increase the risk of falls.

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    Drug Delivery Systems For Neurotrophic Factor Therapy

    Besides GDNF, other neurotrophic factor such as basic fibroblast growth factor have been evaluated. One example involves gelatin nanostructured lipid carriers encapsulating bFGF that can be targeted to the brain via nasal administration . Overall, the nanoformulation stimulated dopaminergic function in surviving synapses and played a neuroprotective role in 6-OHDA hemiparkinsonian rats. A very recent study took advantage of the neuroprotective properties of Activin B, which was administered in a parkinsonian mice using a thermosensitive injectable HG . The biomaterial allowed a sustained protein release over 5 weeks and contributed to substantial cellular protection and behavioral improvement.

    Reasons Parkinsons Disease Can Occur

    Latest developments in symptomatic treatment of Parkinsons disease

    When a loved one is living with Parkinsons, its natural to wonder what caused the disease to take root. Although most cases of Parkisons have an unknown cause, a very small percent of cases can be hereditary . Some studies have linked long-term exposure to pesticides, including one called paraquat, with an increased likelihood of the development of Alzheimers and Parkinsons disease.

    The pesticide was first introduced in the United States in the 1950s and is still used commonly by licensed users today. If you think that your loved one who has been diagnosed with Parkinsons may have been exposed to paraquat, its important that you work with a lawyer to learn whether you may be eligible for compensation. Caring for a loved one with Parkinsons can be costly and time-consuming, especially in the later stages when your loved one requires around-the-clock care. Financial compensation can make it easier to provide your loved one with the care they deserve throughout the progression of the disease.

    Were here to help you decide what to do next after you find out that paraquat exposure may be responsible for the development of Parkinsons disease in your loved one. Reach out to us today for a free case review.

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    A Little Bit Of History

    A new important breakthrough took place in 1983 when Langston and colleagues reported a group of drug users who developed acute parkinsonism after MPTP exposure . These patients developed an acute syndrome indistinguishable from PD. This is due because the MPTP metabolite, MPP+, destroys the dopaminergic neurons in the substantia nigra after a series of alterations in the mitochondrial matrix and the electron transport chain. The SNc of Parkinson patients was also described as exhibiting a marked decrease in complex I activity . The fact that some PD patients have certain polymorphisms in genes that express subunits of complex I suggests that this could be a vulnerability factor in PD . New models based on MPTP intoxication allowed researchers to ascertain PD hallmarks both in vitro and in vivo . Due to the achievements of pharmacological DA treatments, search of cell-based DA replacement approaches were initiated with largely disappointing results . From the surgical and therapeutic point of view, discrete lesions of the BG improved parkinsonism . A monkey model of PD showed motor signs improvement as a result of the chemical destruction of the subthalamic nucleus , with evidence of reversal of experimental parkinsonism by STN lesions. This same year deep brain stimulation of the STN became effective for PD treatment .

    Figure 1. Breakthroughs in Parkinsons disease history.

    New Parkinsons Disease Treatments 2021

    You can legally access new medicines, even if they are not approved in your country.

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    Reasons Parkinson’s Disease Can Occur

    When a loved one is living with Parkinsons, its natural to wonder what caused the disease to take root. Although most cases of Parkison’s have an unknown cause, a very small percent of cases can be hereditary . Some studies have linked long-term exposure to pesticides, including one called paraquat, with an increased likelihood of the development of Alzheimers and Parkinsons disease.

    The pesticide was first introduced in the United States in the 1950s and is still used commonly by licensed users today. If you think that your loved one who has been diagnosed with Parkinsons may have been exposed to paraquat, its important that you work with a lawyer to learn whether you may be eligible for compensation. Caring for a loved one with Parkinsons can be costly and time-consuming, especially in the later stages when your loved one requires around-the-clock care. Financial compensation can make it easier to provide your loved one with the care they deserve throughout the progression of the disease.

    Were here to help you decide what to do next after you find out that paraquat exposure may be responsible for the development of Parkinsons disease in your loved one. Reach out to us today for a free case review.

    New Treatment May Have The Potential To Slow Stop Or Reverse Parkinson Disease

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    Results from a recent study suggest that a revolutionary treatment may have the potential to slow, stop, or even reverse the progression of Parkinson disease.

    Results from a February study of a revolutionary treatment suggest that it may be possible to slow, stop, or even reverse the progression of Parkinson disease, according to findings in the Journal of Parkinsons Disease.

    The 3-part, experimental study investigated whether using a novel delivery system to increase levels of glial cell line-derived neurotrophic factor can regenerate dying dopamine brain cells in patients with Parkinson disease and even reverse their condition. GDNF is a naturally occurring protein that promotes the survival of many types of neurons.

    I believe that this approach could be the first neuro-restorative treatment for people living with Parkinsons, which is, of course, an extremely exciting prospect, Steven Gill, MB, MS, FRCS, who designed the infusion device used in the study, said in a statement.

    Initially, 6 patients enrolled in a pilot study which evaluated the safety of the treatment approach. After the pilot study, 35 additional individuals participated in a subsequent 9-month double-blind trial. Half of the participants were randomly assigned to receive monthly infusions of GDNF while the other half received placebos.

    Reference

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    The History Of Parkinsons

    Parkinsons disease was first defined as a shaking palsy in 1817 by James Parkinson. Half a century later, in 1872, the Parisian neurologist Jean-Martin Charcot coined the term Parkinsons disease.

    Though Parkinson was the first to describe the disease in modern medicine, Charcot and his colleagues revolutionised treatments in the mid-19th century.. Parkinson was a proponent of blood-letting from the neck, in a bid to siphon off inflammatory pathogens and prevent them from reaching the brain. But Charcot and his colleagues favoured pharmaceutical approaches centred around anticholinergic drugs, which block the action of a neurotransmitter called acetylcholine. Anticholinergics are still in use today.

    Around the same time, a host of other treatments were being explored at a hospital in Paris. Hyoscyamine, a plant-derived medication, was put in bread and fed to patients. Other medications, such as a derivative of quinine, were mixed with a syrup of orange rinds.

    Charcot also claimed to see the symptoms of patients with Parkinsons improving when travelling by train and horse-carriage. He became a proponent of vibration therapy, where patients bodies and heads were shaken vigorously by a rigged motor.

    What Diseases And Conditions Resemble Parkinsons Disease

    PD is the most common form of parkinsonism, in which disorders of other causes produce features and symptoms that closely resemble Parkinsons disease. Many disorders can cause symptoms similar to those of PD, including:

    Several diseases, including MSA, CBD, and PSP, are sometimes referred to as Parkinsons-plus diseases because they have the symptoms of PD plus additional features.

    In very rare cases, parkinsonian symptoms may appear in people before the age of 20. This condition is called juvenile parkinsonism. It often begins with dystonia and bradykinesia, and the symptoms often improve with levodopa medication.

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    Clinical Research On Prodromal Parkinsons Disease

    In the clinical situation, manifest PDaccording to Braaket al.is preceded by years, if not decades, by prodromal phases. To screen for prodromal phases, the NMS hyposmia, constipation, depression, and the sleep-dream phase disorder RBD are now considered prodromal indicators. Whereas the first three are sensitive but not specific, RBD is now accepted as the most specific phenotype of the PD prodromal phases with a risk of more than 80% to convert into PD, or dementia with Lewy bodies or less frequently into multiple system atrophyin 10 to 15 years,. Similar research on prodromal stages takes place with at risk relatives of Parkinson patients, who are either heterozygous for theLRRK2 gene or are homozygous for one of the autosomal-recessive genes for a mitochondrial dysfunction in PD or possess a mutation of the gene for glucocerebrosidase 1 and thus are classified as PD-GBA1.

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