Here's more theory including GABA as the problem. It doesn't say GABA in one's diet is a problem or suggest any solution, i.e. it doesn't suggest how to stop the astrocytes:
Quote:The Center for Disease Control and Prevention (CDC) lists complications from Parkinson’s disease as the 14th leading cause of death among Americans....
Surrounding astrocytes (star-shaped non-neuronal cells) in the same region of the brain show an increase in number as the local neurons begin to die off. A key chemical messenger, known as GABA, also starts to increase its levels in the brain. GABA is what stops the dopaminergic neurons from producing dopamine; however, it does not kill them. Parkinson’s disease mechanisms, in its earliest stages of brain change, can allow for dormant neurons to be awakened, and they can resume the production capability of dopamine. The stopping of astrocytes from synthesizing excessive GABA decreases the severity of motor symptoms. Theoretically, addressing Parkinson’s at this early stage can prevent neuronal death of dopamine producers and prevent the disease from occurring at all. This theory is no less than a weighty shift from responsive pharmacological therapy treating symptoms to disease modification or possibly eradication at its root cause.
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It doesn't say how to reduce GABA, nor does it say we need to. It may be more a miss-processing issue. However, this does make one question taking GABA as a supplement.
The critical issue is state in this sentence: "Parkinson’s disease mechanisms, in its earliest stages of brain change, can allow for dormant neurons to be awakened, and they can resume the production capability of dopamine. "
This statement is theoretical, and it therefore, by its very nature, implies the GABA concept is also theoretical.
@sharoncrayn I’m no longer disappointed ☹️ by your theory-busting, rather, I’m a bit liberated- thinking: less research to chase (or feel behind on, with anxiety that I missed the boat). Ah: weeds weeds, everywhere 🙀
Assuming the dormancy theory is valid, then "why" are the dopaminergic neurons dormant in the first place? Does dormancy begin 20-30 earlier as some would suggest? Does everyone get a brain biopsy at 21? If so, what can you do about it?
Is dormancy ... dormancy as we generally considered it, a pause where the neuron's function is muted or invisible. Or is dormancy really a shrinkage of the neuron due to injury that makes it appear dormant and possibly still able to be revived, but cannot be revived?
What if "dormancy" is really all about the breakdown of the dopamine "signalling" pathway because some one forgot to fill in the potholes and turn off the red lights? Then it really doesn't matter if the neuron is dormant or not. Traffic jam of dead cars, stalled cars, overheated cars, cars revving their engines with nowhere to go, etc.
Until it produces something that works, theory has little backing. It's only useful for proposing research. Refuting theories is just as important as substantiating them. Both guide us in the direction to go. It's trying on the patients of those needed a cure now.
Monoamine oxidase inhibitors — known as MAO-B inhibitors — first were used as treatments for depression, but also are useful in treating Parkinson's disease. The drugs block your body's breakdown of the neurotransmitter dopamine in your brain, which helps to keep the dopamine supply higher and to reduce your symptoms of Parkinson's.
The MAO-B inhibitors used most often in Parkinson's include [Safinamide (Xadago)] Eldepryl and Zelapar (selegiline) and Azilect (rasagiline). They can be prescribed alone or with other Parkinson's drugs, and side effects can include nausea, headaches, dry mouth, dizziness, insomnia, and loss of appetite.
Researchers have looked at whether MAO-B inhibitors actually can slow the progression of Parkinson's disease (rather than just improving symptoms), but have concluded there's no evidence of that. Nonetheless, the drugs do help to treat Parkinson's symptoms.
Treatment with two different compounds that block GABA production in astrocytes, called monoamine oxidase-B, or MAO-B, inhibitors, was sufficient for neurons to recover the enzymatic machinery necessary to produce dopamine, the study found. This significantly alleviated Parkinson’s motor symptoms in the study animals.
In fact, the MAO-B inhibitors used for the study — selegiline (brand names Eldepryl, Carbex, Zelapar, among others), and safinamide (brand name Xadago) — are already prescribed to Parkinson’s patients as an add-on therapy to levodopa. They are believed to prevent the break down of dopamine in the brain.
At your link: "Although the results from several clinical trials have cast doubt on the therapeutic efficacy of traditional MAO-B inhibitors, researchers say they have recently developed a new inhibitor, KDS2010. KDS2010 effectively inhibits astrocytic GABA production with minimal side effects in Alzheimer’s animal models and also could be effective for alleviating Parkinson’s motor symptoms, the investigators said."
I am taking Dr. Mischley's class and she's a fan of MAO-B inhibitors as neuroprotective. According to her, the FDA would not come out and endorse because 1 mg of Azilect was shown in studies to slow progression but 2 mg did not, and the FDA could not wrap their arms around this, that a lower dosage was helpful but a larger one was not. So they stopped looking at the study results.
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