China 
Africa 
Explore chapters and articles related to this topic
Cyanobacterial toxins
Published in Ingrid Chorus, Martin Welker, Toxic Cyanobacteria in Water, 2021
An underlying assumption in the BMAA hypothesis of human ALS/PDC effects is that this syndrome encountered in Guam is closely related to other neurodegenerative diseases found globally, but there is evidence contradicting this assumption. Differences between ALS/PDC on Guam and ALS, Parkinsonism and Alzheimer’s diseases include the strong familial occurrence (Zhang et al., 1996; Morris et al., 2001) and the common mixed disease syndrome seen in ALS/PDC on Guam (Murakami, 1999), both situations being extremely rare in the other neurological diseases. Additional characteristics indicating that ALS/PDC is distinct from sporadic ALS, Parkinsonism and Alzheimer’s disease include the absence of beta-amyloid plaques that are characteristic of Alzheimer’s disease, the absence of ubiquitinated Lewy bodies characteristic of Parkinsonism (Hirano et al., 1961), as well as the absence of the typical ALS/PDC tauopathy in sporadic ALS (Ikemoto, 2000). The individual symptomologies exhibited in ALS/PDC cases have been related to differences in the areas of the central nervous system where the highest densities of the aberrant tau proteins occurred (Hof et al., 1994; Umahara et al., 1994). One other significant difference between ALS/PDC and other neurodegenerative diseases is the presence of a retinal pigment epitheliopathy (RPE) that has only been reported in Guam and Kii Peninsula ALS/PDC cases (Kokubo et al., 2003). The condition manifests itself as linear tracks of retinal depigmentation with intermittent pigment clumping, and the incidence of RPE is significantly higher in ALS/PDC cases than in controls. RPE has not been associated with other diseases elsewhere in the world and is therefore considered part of the ALS/PDC disease postulated to be caused by β-methylamino-alanine (BMAA) (Cox et al., 1989; Steele et al., 2015).
Investigating sensitivity coefficients characterizing the response of a model of tau protein transport in an axon to model parameters
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2019
Ivan A. Kuznetsov, Andrey V. Kuznetsov
One of the hallmarks of Alzheimer’s disease (AD) is the formation of insoluble neurofibrillary tangles (NFTs) composed of tau protein (Ballatore et al. 2007; Tai et al. 2012; Ittner et al. 2011; Bloom 2014). Some recent research suggests that abnormalities in axonal transport precede NFT formation and any clinical symptoms of AD (Moreno et al. 2016). The relevance to AD explains the importance of understanding and modeling tau transport in neurons. This is especially important because tau and its interaction with microtubules (MTs) have been identified as a possible therapeutic target in AD (Boutajangout et al. 2011; Pachima et al. 2016; Lippens et al. 2016). For example, DeVos et al. (2017) presented evidence that tau reduction therapy can reverse tau seeding capability in aged mice with tauopathy.
A quantitative risk assessment for chronic traumatic encephalopathy (CTE) in football: How public health science evaluates evidence
Published in Human and Ecological Risk Assessment: An International Journal, 2019
Adam M. Finkel, Kevin F. Bieniek
According to the 2017 Berlin Consensus Statement on Concussion in Sports by 36 neuroscientists, “chronic traumatic encephalopathy (CTE)… appears to represent a distinct tauopathy with an unknown incidence in athletic populations” (McCrory et al.2017). The term “tauopathy” refers to one of several neurodegenerative diseases, including frontotemporal lobar degeneration (FTLD) and progressive supranuclear palsy (PSP), in which the protein tau (found in normal human brain) becomes abnormally aggregated and forms inclusion bodies within nerve and glial cells in the brain. The abnormal tau becomes burdened by an excess of phosphate groups (hyperphosphorylation). A frequent inclusion body containing abnormal and insoluble tau is the “neurofibrillary tangle,” a lesion most often seen in the Alzheimer's disease (AD) brain.14AD also involves aggregation of hyperphosphorylated tau, but because its primary hallmark is the accumulation of fibrils of amyloid protein within plaques, it is considered a “secondary tauopathy.” CTE per se (when not co-existing with AD) does not display amyloid accumulation. In CTE, these tangles accumulate in a characteristic pattern that is different from AD and other tauopathies. A consensus conference of neuropathologists, sponsored by the National Institutes of Health, defined the pathognomonic lesion of CTE as hyperphosphorylated tau aggregates in neurons, astrocytes, and cell processes around small vessels in an irregular pattern at the depths of the cortical sulci (McKee et al.2016). There appear to be two different clinical presentations of CTE (Stern et al.2013); some cases begin relatively early in life (ages 30–50) and involve behavioral and mood disturbances with minimal cognitive impairment, while others begin later in life and display marked cognitive impairment and often motor disturbances as well.
Epigenetic modifications associated with pathophysiological effects of lead exposure
Published in Journal of Environmental Science and Health, Part C, 2019
Madiha Khalid, Mohammad Abdollahi
Tauopathy belongs to a class of neurodegenerative diseases characterized by high levels of tau proteins in the brain, though an appropriate amount of tau proteins is required for stabilizing microtubules.236 Several animal studies have reported the risks of tauopathies associated with developmental Pb exposure via inducing tau phosphorylation and aberrant miRNAs expression.75,237,238 Postnatal 0.2% Pb exposure in transgenic mice carrying human tau gene showed hyperphosphorylated internal and external brain capsules along phosphorylated tau at sites Ser396 protein at PND20/30 (P < 0.001), increased total tau protein at PND20/40 (P = 0.01) and cyclin-dependent kinase 5 (CDK5) protein at PND40/60 (P < 0.001). Increased miR-34c expression was observed between PND20/50 (P = 0.037).237 Similarly, in another study with the same postnatal 0.2% Pb exposure level in mice demonstrated varied miRNAs expression levels over time. At PND20, transient increase in miR-106b (1.5fold) was found unsustainable while, a significant decrease in miR-34c (1.6fold) was found to be sustainable throughout animal life. Moreover, decreased expression of miR-124 was observed at PND700 (2fold), while increased expression was observed of miR-29b at PND20 (1.6fold).76 Among miRNAs whose expression changed with exposure to Pb, miR-34c is known to target microtubule-associated protein tau (MAPT) mRNA and tends to downregulate its expression,239 miR-106b is known to regulate APP expression during brain development and neuronal differentiation and its decreased expression was reported among AD patients76,240 and both miR-124 and -29 b are known to target Sp1 mRNA.76 Overexpression of miR-29b is linked to a significant reduction in DNMT1/3A/3B. It suppresses cell proliferation via targeting Sp1 and PTEN-AKT signaling pathways.241–245 Moreover, significantly increased Sp1 mRNA levels among AD patients have been reported.246 Another miRNA sensitive to Pb exposure, miR-148a, is known to regulate DNMT1 expression.247,248 miR-132 targets MeCP2 mRNA and its downregulation will cause a translational block on MeCP2, which has a pivotal role in normal nerve cell function.249,250 Aforementioned evidence suggests that Pb is capable of inducing aberrant expression of different miRNAs, thereby negatively affecting tight regulations between epigenetic mechanisms, disrupting normal expression of tau protein, and contributing to tauopathies.