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Professor Exley states that aluminium is the cause of autism and alzheimers
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Hip
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AT what point in the video does Professor Exley state that aluminum is the cause of autism and Alzheimer's?
Hip
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Your thread title is wrong, because Professor Exley does not say that aluminum is the cause of autism. At timecode 11:33 he says:
Linking a given factor like aluminum to a disease is one thing, but then proving that factor is the cause of a given disease is very difficult, and no reputable scientist would claim to have proven a causal connection unless there is sufficient evidence.
So why are you misrepresenting what Professor Exley has said?
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The levels of aluminium in this fifteen year old boy's brain were comparable to that seen in much older people who die with a diagnosis of familial alzheimers. Their brains are also loaded with aluminium. Some of the highest levels seen in a human brain.
Professor Exley said in the beginning of his talk "if there were no aluminium in the brain,there would be no alzheimers".....
Professor Exley said in the beginning of his talk "if there were no aluminium in the brain,there would be no alzheimers".....
The Emperor is Naked: No aluminium, no Alzheimer’s disease. This is the, perhaps unexpected, conclusion of a new open access paper published in Journal of Alzheimer’s Disease Reports. Putting the headline in context what is actually being suggested is that brain content of aluminium is a catalyst for Alzheimer’s disease. In the absence of pathologically significant deposits of aluminium in brain tissue there would not be any (acute) Alzheimer’s disease within a normal lifespan of say 100 years. Support for this conclusion has been building over the last decade or so and has now been put on an unequivocally firm footing by recent research demonstrating the exceedingly high content of aluminium in brain tissue in individuals who died with a diagnosis of familial Alzheimer’s disease.
Individuals with familial Alzheimer’s disease have specific genetic predispositions to Alzheimer’s developing earlier in life, perhaps as early as the fourth or fifth decade of life. All of these genetic predispositions are associated with how the body metabolises the amyloid precursor protein (APP) and yet there is no unequivocal explanation of how APP and its metabolic products, such as amyloid β cause Alzheimer’s disease. The contention in the new research is that these genetic mutations in the metabolism and processing of APP concomitantly act as predispositions to the retention of aluminium in brain tissue. Increased absorption of aluminium across the gut, as is seen in late-onset Alzheimer’s disease and in Down’s syndrome, could contribute to increased retention of aluminium in brain tissue. However, while we do not know the mechanism behind this increased retention what we do know is that when brain aluminium content is increased, and not because of specific genetic mutations but due to environmental or occupational exposure to aluminium, then an earlier form of late-onset or sporadic Alzheimer’s disease will occur.
There are clearly many potential contributory factors in the aetiology of Alzheimer’s disease but what is now being suggested is that without concomitant pathologically-significant deposits of aluminium there would not be any Alzheimer’s disease.
Individuals with familial Alzheimer’s disease have specific genetic predispositions to Alzheimer’s developing earlier in life, perhaps as early as the fourth or fifth decade of life. All of these genetic predispositions are associated with how the body metabolises the amyloid precursor protein (APP) and yet there is no unequivocal explanation of how APP and its metabolic products, such as amyloid β cause Alzheimer’s disease. The contention in the new research is that these genetic mutations in the metabolism and processing of APP concomitantly act as predispositions to the retention of aluminium in brain tissue. Increased absorption of aluminium across the gut, as is seen in late-onset Alzheimer’s disease and in Down’s syndrome, could contribute to increased retention of aluminium in brain tissue. However, while we do not know the mechanism behind this increased retention what we do know is that when brain aluminium content is increased, and not because of specific genetic mutations but due to environmental or occupational exposure to aluminium, then an earlier form of late-onset or sporadic Alzheimer’s disease will occur.
There are clearly many potential contributory factors in the aetiology of Alzheimer’s disease but what is now being suggested is that without concomitant pathologically-significant deposits of aluminium there would not be any Alzheimer’s disease.
Does human exposure to aluminium have a role to play in autism spectrum disorder (ASD)? Research at Keele University published in the Journal of Trace Elements in Medicine and Biology provides the strongest indication yet that aluminium is an aetiological agent in ASD. The aluminium content of brain tissues from 5 donors who died with a diagnosis of ASD was found to be extraordinarily high, some of the highest values yet measured in human brain tissue. Why for example, would the occipital lobe of a 15 year old boy with autism be 8.74 (11.59) micrograms/g dry wt., a value which is at least 10 times higher than might be considered as acceptable for an aged adult never mind a child?
However, while the aluminium content of each of the 5 brains was shockingly high it was the location of the aluminium in the brain tissue which served as the standout observation. The majority of aluminium was identified inside non-neuronal cells including microglia and astrocytes.
However, while the aluminium content of each of the 5 brains was shockingly high it was the location of the aluminium in the brain tissue which served as the standout observation. The majority of aluminium was identified inside non-neuronal cells including microglia and astrocytes.
Aluminium was also found in lymphocytes in the meninges and in similar inflammatory cells in the vasculature. There was clear evidence of inflammatory cells heavily loaded with aluminium entering the brain via the meningeal membranes and the blood-brain-barrier.
The fact that the majority of aluminium found in brain tissues in ASD was intracellular and associated with non-neuronal cells is, at least for now, unique to ASD and may begin to explain why young adolescents had so much aluminium in their brains.
The fact that the majority of aluminium found in brain tissues in ASD was intracellular and associated with non-neuronal cells is, at least for now, unique to ASD and may begin to explain why young adolescents had so much aluminium in their brains.
Perhaps there is something within the genetic make-up of specific individuals which predisposes themto accumulate and retain aluminium in their brain, as is similarly suggested for individuals with familial Alzheimer’s disease. The new evidence strongly suggests that aluminium is entering the brain in ASD via pro-inflammatory cells which have become loaded up with aluminium in the blood and/or lymph, much as has been demonstrated for monocytes at injection sites for vaccines including aluminium adjuvants. Perhaps we now have the putative link between vaccination and ASD, the link being the inclusion of an aluminium adjuvant in the vaccine.
Professor Chris Exley
Professor in Bioinorganic Chemistry Keele University
Honorary Professor, UHI Millennium Institute
Group Leader - Bioinorganic Chemistry Laboratory at Keele
However, while the aluminium content of each of the 5 brains was shockingly high it was the location of the aluminium in the brain tissue which served as the standout observation. The majority of aluminium was identified inside non-neuronal cells including microglia and astrocytes.
However, while the aluminium content of each of the 5 brains was shockingly high it was the location of the aluminium in the brain tissue which served as the standout observation. The majority of aluminium was identified inside non-neuronal cells including microglia and astrocytes.
Aluminium was also found in lymphocytes in the meninges and in similar inflammatory cells in the vasculature. There was clear evidence of inflammatory cells heavily loaded with aluminium entering the brain via the meningeal membranes and the blood-brain-barrier.
The fact that the majority of aluminium found in brain tissues in ASD was intracellular and associated with non-neuronal cells is, at least for now, unique to ASD and may begin to explain why young adolescents had so much aluminium in their brains.
The fact that the majority of aluminium found in brain tissues in ASD was intracellular and associated with non-neuronal cells is, at least for now, unique to ASD and may begin to explain why young adolescents had so much aluminium in their brains.
Perhaps there is something within the genetic make-up of specific individuals which predisposes themto accumulate and retain aluminium in their brain, as is similarly suggested for individuals with familial Alzheimer’s disease. The new evidence strongly suggests that aluminium is entering the brain in ASD via pro-inflammatory cells which have become loaded up with aluminium in the blood and/or lymph, much as has been demonstrated for monocytes at injection sites for vaccines including aluminium adjuvants. Perhaps we now have the putative link between vaccination and ASD, the link being the inclusion of an aluminium adjuvant in the vaccine.
Professor Chris Exley
Professor in Bioinorganic Chemistry Keele University
Honorary Professor, UHI Millennium Institute
Group Leader - Bioinorganic Chemistry Laboratory at Keele
Hip
Senior Member
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That's not the same as saying aluminum causes Alzheimer's.
With aluminum in the brain of Alzheimer's patients, nobody knows whether that's the cause or consequence of Alzheimer's.