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2018 ; 9
(ä): 74
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Immunoexcitotoxicity as the central mechanism of etiopathology and treatment of
autism spectrum disorders: A possible role of fluoride and aluminum
#MMPMID29721353
Strunecka A
; Blaylock RL
; Patocka J
; Strunecky O
Surg Neurol Int
2018[]; 9
(ä): 74
PMID29721353
show ga
Our review suggests that most autism spectrum disorder (ASD) risk factors are
connected, either directly or indirectly, to immunoexcitotoxicity. Chronic brain
inflammation is known to enhance the sensitivity of glutamate receptors and
interfere with glutamate removal from the extraneuronal space, where it can
trigger excitotoxicity over a prolonged period. Neuroscience studies have clearly
shown that sequential systemic immune stimulation can activate the brain's immune
system, microglia, and astrocytes, and that with initial immune stimulation,
there occurs CNS microglial priming. Children are exposed to such sequential
immune stimulation via a growing number of environmental excitotoxins, vaccines,
and persistent viral infections. We demonstrate that fluoride and aluminum
(Al(3+)) can exacerbate the pathological problems by worsening excitotoxicity and
inflammation. While Al(3+) appears among the key suspicious factors of ASD,
fluoride is rarely recognized as a causative culprit. A long-term burden of these
ubiquitous toxins has several health effects with a striking resemblance to the
symptoms of ASD. In addition, their synergistic action in molecules of
aluminofluoride complexes can affect cell signaling, neurodevelopment, and CNS
functions at several times lower concentrations than either Al(3+) or fluoride
acting alone. Our review opens the door to a number of new treatment modes that
naturally reduce excitotoxicity and microglial priming.