Wyniki wyszukiwania - Biblioteka Nauki

1

An evaluation of the role and treatment of elevated male hormones in autism spectrum disorders

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Geier D. A. , Kern J. K. , King P. G. , Sykes L. K. , Geier M. R.

Acta Neurobiologiae Experimentalis

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2012

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tom 72

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nr 1

EN

Autism, Asperger's syndrome (AS), and pervasive developmental disorder - not otherwise specified (PDD-NOS) compose the overall diagnostic category of autism spectrum disorder (ASD). Subjects diagnosed with an ASD have a male:female ratio of 4:1, and among subjects diagnosed with AS the male:female ratio is as high as 9:1. The purpose of this study was to examine evidence of the association between hyperandrogenism and autistic traits (ATs) among subjects diagnosed with an ASD, and to evaluate the effectiveness of anti-androgen therapy as a means to help treat ATs in subjects diagnosed with an ASD. Evidence of hyperandrogenism in subjects diagnosed with an ASD is supported by multiple studies in the areas of psychological framework, brain pathology, tissue culture, and pre- and postnatal androgen levels. Data from subjects diagnosed with other conditions associated with elevated androgens reveals many of these individuals have ATs. Finally, in a placebo-controlled trial of testosterone administration to neurotypical subjects, testosterone was found to increase ATs. In addition, a controlled trial of human transsexuals revealed a significant increase in ATs in female-to-male transsexuals and a decrease in ATs in male-to-female transsexuals. Data from multiple animals and human clinical trials suggest that anti- androgen medications have the ability to significantly reduce ATs in patients diagnosed with an ASD. In light of the robust association between hyperandrogenism and ASD, it is recommended subjects diagnosed with an ASD should undergo routine screening for elevated androgens, and appropriate treatment should be initiated for those with elevated androgens.

2

Evidence of parallels between mercury intoxication and the brain pathology in autism

86%

Kern J. K. , Geier D. A. , Audhya T. , King P. G. , Sykes L. K. , Geier M. R.

Acta Neurobiologiae Experimentalis

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2012

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tom 72

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nr 2

EN

The purpose of this review is to examine the parallels between the effects mercury intoxication on the brain and the brain pathology found in autism spectrum disorder (ASD). This review finds evidence of many parallels between the two, including: (1) microtubule degeneration, specifically large, long-range axon degeneration with subsequent abortive axonal sprouting (short, thin axons); (2) dentritic overgrowth; (3) neuroinflammation; (4) microglial/astrocytic activation; (5) brain immune response activation; (6) elevated glial fibrillary acidic protein; (7) oxidative stress and lipid peroxidation; (8) decreased reduced glutathione levels and elevated oxidized glutathione; (9) mitochondrial dysfunction; (10) disruption in calcium homeostasis and signaling; (11) inhibition of glutamic acid decarboxylase (GAD) activity; (12) disruption of GABAergic and glutamatergic homeostasis; (13) inhibition of IGF-1 and methionine synthase activity; (14) impairment in methylation; (15) vascular endothelial cell dysfunction and pathological changes of the blood vessels; (16) decreased cerebral/cerebellar blood flow; (17) increased amyloid precursor protein; (18) loss of granule and Purkinje neurons in the cerebellum; (19) increased pro-inflammatory cytokine levels in the brain (TNF-a, IFN-y, IL-ip, IL-8); and (20) aberrant nuclear factor kappa-light-chain-enhancer of activated B cells (NF-KB). This review also discusses the ability of mercury to potentiate and work synergistically with other toxins and pathogens in a way that may contribute to the brain pathology in ASD. The evidence suggests that mercury may be either causal or contributory in the brain pathology in ASD, possibly working synergistically with other toxic compounds or pathogens to produce the brain pathology observed in those diagnosed with an ASD.

3

Developmental neurotoxicants and the vulnerable male brain: a systematic review of suspected neurotoxicants that disproportionally affect males

86%

Kern J. K. , Geier D. A. , Homme K. G. , King P. G. , Bjorklund G. , Chirumbolo S. , Geier M. R.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr 4

EN

The prevalence of neurodevelopmental disorders (NDs), including autism spectrum disorder, attention‑deficit/hyperactivity disorder, tic disorder, obsessive‑compulsive disorder, and emotional disturbances, has increased notably in the past few decades. To date, debate continues as to the origins of NDs. Increases in widespread exposure to and bioaccumulation of chemical neurotoxicants have paralleled the upsurge in NDs, and are suggested to be causal agents for NDs. One consistent aspect of NDs is the male preponderance. This review considers the issue of male preponderance by reviewing the gender‑specific neurotoxic effects of recognized neurotoxicant chemicals to assess their possible etiology in NDs. This investigation consisted of a systematic literature review of original studies published from 1970–2016 on suspected neurotoxicants, to examine whether they have a disproportionate adverse effect based on gender. Based on that review, the neurotoxicants exhibiting consistent gender‑specific effects, with exposed males being more affected (than similarly exposed females), were: lead, Thimerosal/ethylmercury, some organochlorine pesticides (e.g., dieldrin, endosulfan, and heptachlor), and air pollution. The next group identified were neurotoxicants exhibiting gender‑specific neurotoxic effects, with males being somewhat (but not consistently) more affected than females: mercury vapor, polychlorinated biphenyls (PCBs), and organophosphate pesticides. Finally, there was a group of studies in which the neurotoxicants exhibited apparent gender‑related neurotoxic effects but failed to show whether exposed males were consistently more affected than females: inorganic mercury salts, methylmercury species, and certain endocrine disruptors (e.g., phthalates and BPA). The overall conclusion from the studies reviewed was that the brain in males is more vulnerable to many toxic exposures than it is in females. Evidence suggests that the reasons for the male brain being more vulnerable include: (1) greater glutathione availability in females; (2) greater sulfate‑based detoxification capacity in females; (3) potentiating effects of co‑exposure to neurotoxicants and testosterone; (4) greater neuroinflammatory response in males; (5) reduced vulnerability to oxidative stress in females; and (6) neuroprotective effects of female hormones (estrogen and progesterone), especially in the reduction of inflammation and oxidative stress.