Despite recent advances in the treatment of Parkinson's disease (PD), dyskinesia and motor fluctuations still make a substantial contribution to the reduced quality of life of patients with advanced-stage PD. Additionally, non-motor signs such as depression, dementia, sleep abnormalities and autonomic failure are increasingly being recognized as challenges to effective treatment as they dominate the clinical, caregiver and financial burden of the later stages of PD.
The translational value of current preclinical models of neurodegeneration remains unsatisfactory. Current limitations could be overcome in a number of ways; for example, by obtaining combinations of mutations by breeding mice with single or dual mutations, or by challenging existing models with environmental stressors such as neurotoxins or neuroinflammation inducers in animals with an established and stable background.
Novel drug targets will be uncovered through pathophysiological insights gained from the identification of the role of genetic mutations that are responsible for hereditary forms of PD, and future therapies targeted towards these mutations will have broader efficacy against sporadic PD than the currently available symptomatic treatments.
Many of the therapies that are currently under development — both dopaminergic and non-dopaminergic compounds — are focused on improving motor control, fluctuations and dyskinesias. Far fewer approaches address the other two key unmet clinical needs: specifically, alleviating non-motor symptoms, and disease modification and/or neuroprotection.
The most promising strategy to achieve disease modification or neuroprotection seems to be a combination of compounds that interfere simultaneously with different key events of PD pathology. This approach would require collaboration between the pharmaceutical companies that hold the patent rights of the different compounds.
Primary end points in past and ongoing trials of potential disease-modifying or neuroprotective drugs rely on clinical assessment scales. Additional efforts are therefore urgently needed to establish validated biomarkers in PD.
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pvw2
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Excuse me for being a cynic. I have had the good fortune to have reversed most of my movement symptoms and to no longer need to take any Pd medication,
I understand the medical profession and the drugs industry only looking for a medical way to reverse Parkinson's symptoms, but they have not yet been very successful and they have invested billions in their attempts.
Nobody is interested in a non-medical solution to our problems, other than us, the patients. We are not going to hear any support for the FAST WALKING, which is what I do, because it does not put any money into anybody's pockets. I don't blame them, I would probably do the same in their position.
But YOU, the patient should be aware of what you can do to help yourself reverse many of your symptoms. I don't charge anybody for doing what I do, I give it to them free of charge, Yes I have a book out there on the subject, which needs constant updates and costs money to print, but it is not compulsory for you to buy one, I will help you as much as I can,
I have also written two other books on my life, both before and after Pd. Those are also available on Amazon, but their purpose is to let you know that I am just a very ordinary person, who has very little formal education and no qualifications whatsoever. But I did become a very successful businessman and I did overcome most of my Pd symptoms. It just goes to show what we are all capable of, if we could only have the faith in ourselves to be able to try to succeed.
You are demonstrating what my neurologist said about PD. The theory is exercise produces glutathione. Thus, a good diet with the glutathione building blocks is also important and adequate sleep.
Quote: But what has been proven? There is compelling scientific evidence in animal models of PD that intensive exercise can alter the way the brain works and promote recovery. Research at the University of Southern California (USC) shows how exercise improves walking and other motor skills in people with PD. It is also shedding light on how exercise influences neuroplasticity at the molecular level.
There are a lot of articles that have appeared on HU but I will battle to find them all but here goes:
When we exercise our bodies and brains produce various chemicals which repair damaged cells. Glial Derived Neurotrophic factor (GDNF) is the most important as far as I am concerned, but others also help. GDNF as the name implies, repairs the damaged GLIAL cells, which are responsible for the production of Dopamine. Need I tell you more.
The articles on GDNF and BDNF relate to the result of doing exercise.
Glial Derived Neurotrophic Factor (GDNF) repairs or replaces damaged brain cells, in other words we have our own repair kit for Pd.
Notably, vigorous exercise in these parkinsonian animal models induces brain neurotrophic factor expression, which may mediate putative neuroprotective effects. This includes brain-derived neurotrophic factor (BDNF)47 and glial-derived neurotrophic factor (GDNF).47,51 Note that both BDNF and GDNF are significantly reduced in the substantia nigra of patients with PD.59 One other animal model utilized systemically administered lipopolysaccharide to induce nigral cell loss and parkinsonism; exercise blocked these negative outcomes in proportion to the exercise duration, apparently mediated by elevated BDNF levels.60 Other exercise effects in parkinsonian animal models have included enhanced subventricular zone neural progenitor cell proliferation and migration,47 as well as reversal of age-related decline in substantia nigra vascularization, apparently mediated by vascular endothelial growth factor (VEGF) expression.e1
Increased expression of the neuroprotective agent, insulin-like growth factor I, which interacts with BDNF to mediate exercise-induced cognitive gainse15; exercise-induced production of this factor protects against neurotoxic hippocampal insultse16 and is acutely elevated by exercise in normal humanse17
A couple of days ago, my husband had his annual appointment with his MDS at Vanderbilt. He told us that "Meds are for symptomatic relief, EXERCISE slows progression." He pushed no meds and asked my husband if he still takes MP. His nurse wrote down ALL his vitamins/supplements into such a detail, I was amazed. His pull test was a half step back, the doctor was very pleased and asked us to make an appointment to return in a year.
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