RETRACTED ARTICLE: Aluminum in Neurological and Neurodegenerative Disease

Abstract

WJL aided in the acquisition of all brain tissues and performed all analytical experiments involving ETAAS and XRFR and assisted to interpret and analyze all data; PNA, ZF, AIP, YZ, WL and WJL collected, archived, organized, and tabulated all data and performed statistical analysis; AIP and WJL wrote the paper. Compliance with Ethical Standards Ethics Statement All acquisition, handling, experimental, and analytical procedures involving postmortem human brain tissues were carried out in an ethical manner in strict accordance with the ethics review board policies at brain and tissue donor institutions and at the Louisiana State University (LSU) Health Sciences Center. Informed consent from next of kin was obtained at brain and tissue donor institutions for all tissue samples prior to autopsy and donation; coded postmortem brain tissue samples (containing no personal identifying information of the donors) were obtained from the 18 brain and tissue banks listed in the Acknowledgements section above. The ethical use of postmortem human brain tissues and their analyses were also carried out in strict accordance with the Institutional Biosafety Committee and the Institutional Review Board Committee (IBC/IRBC

Heavy metals contaminating the environment of a progressive supranuclear palsy cluster induce tau accumulation and cell death in cultured neurons

“…On the other hand, the treatment with aluminum, a heavy metal not enriched in the environment of Wattrelos, did not induce cytotoxicity in iNeurons. Together, these results suggest that Cr and Ni exposure, but not other heavy metals such as Al, could be potentially associated with the sporadic PSP cluster found in Wattrelos and support previous studies suggesting that Al and Cd exposure is associated with some neurodegenerative diseases such as AD, but not with PSP 19,58,59 . www.nature.com/scientificreports www.nature.com/scientificreports/ We also studied the cell death induced by chromium and nickel in SH-SY5Y neuroblastoma cells, a well-known dopaminergic neuronal-like cell model previously used to study neurotoxicity 60,61 .…”

The Nutritional Components of Beer and Its Relationship with Neurodegeneration and Alzheimer’s Disease

“…According to Kawahara [32], this metal induces in vivo as well as in vitro neuronal apoptosis. Aluminum may play an active role in the pathogenesis of critical neuropathologic lesions in Alzheimer’s disease and other related disorders, through cross-linking hyperphosphorylated proteins [33,34]. In fact, Al-induced Alzheimer-like pathological changes were first attributed to tau proteins.…”

Linking Molecular Pathways and Large-Scale Computational Modeling to Assess Candidate Disease Mechanisms and Pharmacodynamics in Alzheimer's Disease

“…The goal of the present study is to incorporate the hypothesized qualitative and quantitative effects of Abeta on neuronal population dynamics into our brain network models, i.e., adding mathematical models that describe how molecular changes alter population activity—so called cause-and-effect models. We will focus here on the disrupted inhibitory function of interneurons and consecutive hyperexcitability caused by Abeta—while we are aware of various other factors with potential roles for AD etiology, such as vascular changes (Love and Miners, 2016; Storck and Pietrzik Claus, 2018; Bannai et al, 2019), neuroinflammation (Heneka et al, 2015a,b; Wang and Colonna, 2019; Zhou et al, 2019), genetics (Mahley, 2016; Hudry et al, 2019; Takatori et al, 2019), environmental factors (Alonso et al, 2018; McLachlan et al, 2019) and concomitant proteinopathies others than Abeta pathology (Robinson et al, 2018a,b). Beside Abeta there is a second molecular hallmark associated with the pathogenesis of AD: the phosphorylated Tau “tubulin-associated unit” protein (Bloom, 2014; Guo et al, 2017; Tapia-Rojas et al, 2019) which contributes to microtubule stability in the neural cytoskeleton (Guo et al, 2017).…”