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Parkinson's disease begins as an PHOTOelectrical defect.......

Discussion in 'Educating Doctors' started by Jack Kruse, Jan 6, 2019.

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  1. Jack Kruse

    Jack Kruse Administrator

  2. Jack Kruse

    Jack Kruse Administrator

    ^^^^^^the brain compensates for the shortage of signals (DC electric current and dopamine in neurons) by creating additional dopamine receptors. This sensitizes the system to decreased production of the neurotransmitter. This has a positive effect initially, but if the environment does not revert back to normality, a chronic stimulus stimulates apoptosis and cell death via a variety of mechanisms. As cell death progresses further, the correct signal from a normal environment may not be able to elicit the same response, and eventually, the coupled system extincts the response and may disappear. At this stage, the compensation becomes so overwhelming in the coupled feedback loop that even small variations in the level of dopamine trigger the stop signal – which can therefore cause the patient to develop the disease. This is why taking dopamine drugs long-term with no environmental change is very unwise.

    Many biological systems spontaneously organize themselves if they are forced away from thermodynamic equilibrium. This is how Nature uses the chaos of environmental signals to build order. If the organism is not facing a natural environment a system based on Nature will always fall back toward an equilibrium bias and die off or succumb to disease. This can occur from a lack of sun and/or an overdose of manufactured light or radiation from other unknown origins
    Richard Watson likes this.
  3. Jack Kruse

    Jack Kruse Administrator

    It’s been known for decades that mitochondria have an intimate relationship with the nucleus, where most of the genes for mitochondrial proteins reside. Yet it’s becoming apparent that mitochondria also have numerous interactions with other organelles.

    Studies of networks of mitochondria are already yielding insights into some diseases. For instance, some scientists suspect that defective energy metabolism plays a role in Parkinson’s disease, but so far, no clear difference has been found between the neuronal mitochondria of patients and healthy people. But a research team led by Feng He of the Luxembourg Institute of Health recently directed a computer to crunch through 700 gigabytes’ worth of microscopy videos of gut neurons from Parkinson’s disease patients. The system identified nearly 20 features that mathematically characterized the mitochondrial networks in their cells in terms of the organelles’ density, proximity to one another, and interactions. The study, which examined only a small number of patients, found that the features could collectively differentiate patients from healthy people. To He, it seems that mitochondrial networks in Parkinson’s disease might be less efficient and that this inefficiency could contribute to the disease. By capturing layers of biology that more reductionist approaches tend to miss, such network studies could “reshape [our understanding] of different cell types in our body,” he said.
    JanSz likes this.
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