Inhibition of sheep brain acetylcholinesterase by hexachlorophene

Gv, Prasad; Indira, K.; Rajendra, Wudayagiri

doi:10.1007/bf01606571

Cited by 3 publications

(1 citation statement)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In vitro studies on the effects of HCP exposure on the murine brain showed decreased activity of brain succinate dehydrogenase [ 153 ]. Studies on sheep supported the finding that HCP causes changes in brain metabolism [ 154 ]. Since the use of HCP was prevalent prior to 1973, studies using premature infant brains and follow-up work in children showed vacuolar encephalopathy after intensive exposures of prematurely and newly born infants [ 155 , 156 ] from repeated whole body bathing using formulations containing 3% HCP.…”

Section: Antimicrobialsmentioning

confidence: 84%

Role of Environmental Contaminants in the Etiology of Alzheimer’s Disease: A Review

Yegambaram

Manivannan

Beach

et al. 2015

CAR

231

120

View full text Add to dashboard Cite

Alzheimer's dis ease (AD) is a leading cause of mortality in the developed world with 70% risk attributable to genetics. The remaining 30% of AD risk is hypothesized to include environmental factors and human lifestyle patterns. Environmental factors possibly include inorganic and organic hazards, exposure to toxic metals (aluminium, copper), pesticides (organochlorine and organophosphate insecticides), industrial chemicals (flame retardants) and air pollutants (particulate matter). Long term exposures to these environmental contaminants together with bioaccumulation over an individual's life-time are speculated to induce neuroinflammation and neuropathology paving the way for developing AD. Epidemiologic associations between environmental contaminant exposures and AD are still limited. However, many in vitro and animal studies have identified toxic effects of environmental contaminants at the cellular level, revealing alterations of pathways and metabolisms associated with AD that warrant further investigations. This review provides an overview of in vitro, animal and epidemiological studies on the etiology of AD, highlighting available data supportive of the long hypothesized link between toxic environmental exposures and development of AD pathology.

show abstract