[zanpar321]

I do believe this theory really has legs folks!

A study performed in 2015 with green monkey subjects found that animals orally administered BMAA developed hallmark histopathology features of Alzheimer's Disease including amyloid beta plaques and neurofibrillary tangle accumulation. Animal subjects in the trial fed smaller doses of BMAA were found to have correlative decreases in these pathology features. Additionally, animals that were co-administered BMAA with serine were found to have 70% less beta-amyloid plaques and neurofibrillary tangles than those administered BMAA alone, suggesting that serine may be protective against the neurotoxic effects of BMAA. This experiment represents the first in-vivo model of Alzheimer's Disease that features both beta-amyloid plaques and hyperphosphorylated tau protein. This study also demonstrates that BMAA, an environmental toxin, can trigger neurodegenerative disease.[16]

BMAA may also misincorporate into nascent proteins in place of L-serine, possibly causing protein misfolding and aggregation, both hallmarks of tangle diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), progressive supranuclear palsy (PSP), and Lewy body disease. In vitro research has shown that protein association of BMAA can be inhibited in presence of excess L-serine.

BMAA bacteria can be found in water, lakes, seafood etc.

https://en.wikipedia.org/wiki/Beta-M...mino-L-alanine

[GerryW]

Originally Posted by zanpar321

I do believe this theory really has legs folks!

A study performed in 2015 with green monkey subjects found that animals orally administered BMAA developed hallmark histopathology features of Alzheimer's Disease including amyloid beta plaques and neurofibrillary tangle accumulation. Animal subjects in the trial fed smaller doses of BMAA were found to have correlative decreases in these pathology features. Additionally, animals that were co-administered BMAA with serine were found to have 70% less beta-amyloid plaques and neurofibrillary tangles than those administered BMAA alone, suggesting that serine may be protective against the neurotoxic effects of BMAA. This experiment represents the first in-vivo model of Alzheimer's Disease that features both beta-amyloid plaques and hyperphosphorylated tau protein. This study also demonstrates that BMAA, an environmental toxin, can trigger neurodegenerative disease.[16]

BMAA may also misincorporate i with numerous causesnto nascent proteins in place of L-serine, possibly causing protein misfolding and aggregation, both hallmarks of tangle diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), progressive supranuclear palsy (PSP), and Lewy body disease. In vitro research has shown that protein association of BMAA can be inhibited in presence of excess L-serine.

BMAA bacteria can be found in water, lakes, seafood etc.

https://en.wikipedia.org/wiki/Beta-M...mino-L-alanine

Like a lot of people, I think idiopathic PD is a set of symptoms with numerous causes, sort of like a headache. It just happens that the dopamine producing neurons are easily damaged but they are not the only ones, hence the variety of symptoms.

Some proposed causes are misfolded alpha-synuclein protein, environmental toxins such as pesticides/herbicides or industrial solvents, excess iron or manganese, vitamin B2, B6, B1 or D3 deficiency, prion disease, autoimmune condition, an imbalance of neurotransmitters, various infections and related toxins such as cyanobacteria (blue green algae), Lyme disease, Nocardia asteroides, Giardia lamblia, Candida albicans, Helicobacter pylori, Chlamydia pneumoniae, and CMV, EBV, HSV-1 viruses. Oxygen deprivation from arterial compression in the spine or neck vertebrae as well as the brain's peduncle, abnormal chi flow from a foot injury, neck injury, misaligned jaw, arteries irritating the brain, dysbiosis, and aging are some other things that can bring on Parkinsonism. Many people have found relief by attending to one of these causes. So PD symptoms can be caused by a lot of things and that makes finding a cure complicated. What works for one person may not work for another.

The current focus on alpha-synuclein misfolding may not be relevant to everyone and it might not be the only mechanism of cell damage.

[zanpar321]

Originally Posted by GerryW

Like a lot of people, I think idiopathic PD is a set of symptoms with numerous causes, sort of like a headache. It just happens that the dopamine producing neurons are easily damaged but they are not the only ones, hence the variety of symptoms.

Some proposed causes are misfolded alpha-synuclein protein, environmental toxins such as pesticides/herbicides or industrial solvents, excess iron or manganese, vitamin B2, B6, B1 or D3 deficiency, prion disease, autoimmune condition, an imbalance of neurotransmitters, various infections and related toxins such as cyanobacteria (blue green algae), Lyme disease, Nocardia asteroides, Giardia lamblia, Candida albicans, Helicobacter pylori, Chlamydia pneumoniae, and CMV, EBV, HSV-1 viruses. Oxygen deprivation from arterial compression in the spine or neck vertebrae as well as the brain's peduncle, abnormal chi flow from a foot injury, neck injury, misaligned jaw, arteries irritating the brain, dysbiosis, and aging are some other things that can bring on Parkinsonism. Many people have found relief by attending to one of these causes. So PD symptoms can be caused by a lot of things and that makes finding a cure complicated. What works for one person may not work for another.

The current focus on alpha-synuclein misfolding may not be relevant to everyone and it might not be the only mechanism of cell damage.

The Non-Protein Amino Acid BMAA Is Misincorporated into Human Proteins in Place of l-Serine Causing Protein Misfolding and Aggregation

Mechanisms of protein misfolding are of increasing interest in the aetiology of neurodegenerative diseases characterized by protein aggregation and tangles including Amyotrophic Lateral Sclerosis (ALS), Alzheimer’s disease (AD), Parkinson’s disease (PD), Lewy Body Dementia (LBD), and Progressive Supranuclear Palsy (PSP). Some forms of neurodegenerative illness are associated with mutations in genes which control assembly of disease related proteins.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783393/

[kiwi33]

I think that GerryW has made a very good point.

A while ago I listened to a talk at a scientific conference, given by a PD expert from Cambridge with both a medical degree and a PhD (impressive!).

His view is that almost certainly PD is not "one disease" - rather, the causal factors differ from person to person, leading to some common neurological effects.

[zanpar321]

Originally Posted by kiwi33

I think that GerryW has made a very good point.

A while ago I listened to a talk at a scientific conference, given by a PD expert from Cambridge with both a medical degree and a PhD (impressive!).

His view is that almost certainly PD is not "one disease" - rather, the causal factors differ from person to person, leading to some common neurological effects.

I agree with Gerry. Likely more than one cause is behind the emergence of PD. Perhaps whatever the catylist, at some point the neurons in the brain become faulty and die. That may be the one commonality that all PD patients share. The dead brain cells. Some brain cells may be damaged by BMAA bacteria, others due to traumatic injury (e.d. Ali), some due to welding fumes etc. If only there was some way to clear out the dead/faulty cells and grow new neurons!

[jeffreyn]

zanpar321 said: "If only there was some way to clear out the dead/faulty cells and grow new neurons!"

I think the "grow new neurons" bit is still looking promising, via, for example, neural grafting.

The World Parkinson Coalition recently did a podcast (approx. 27 minutes) on this topic on SoundCloud. I can't include links in my posts yet, but if you Google "11 New Neurons for Old" it should be top of the list.