Developmental exposure to lead (Pb) alters the expression of the human tau gene and its products in a transgenic animal model

NeuroToxicology

Volumn 55, Issue , 2016, Pages 154-159

  Dash, M ^a   Eid, A ^a   Subaiea, G ^b   Chang, J ^a   Deeb, R ^a   Masoud, A ^a,c   Renehan, W E ^a   Adem, A ^d   Zawia, N H ^a  

^a UNIVERSITY OF RHODE ISLAND   (United States)

^b UNIVERSITY OF HAIL   (Saudi Arabia)

^c THAMAR UNIVERSITY   (Yemen)

^d UNITED ARAB EMIRATES UNIVERSITY   (United Arab Emirates)

Author keywords

Alzheimer's disease; Lead; MicroRNA; Neurofibrillary tangles; Tauopathy

Indexed keywords

CYCLIN DEPENDENT KINASE 5; LEAD; MESSENGER RNA; MICRORNA; MICRORNA 34C; SERINE; TAU PROTEIN; UNCLASSIFIED DRUG; GREEN FLUORESCENT PROTEIN; MAPT PROTEIN, HUMAN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BRAIN CORTEX; BRAIN LEVEL; CONTROLLED STUDY; GENE EXPRESSION; GENOTYPING TECHNIQUE; IMMUNOHISTOCHEMISTRY; MOUSE; MOUSE MODEL; MOUSE MUTANT; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; TAU GENE; TRANSGENE; TRANSGENIC MOUSE; UPREGULATION; WESTERN BLOTTING; ANIMAL; DOSE RESPONSE; DRUG EFFECTS; GENE EXPRESSION REGULATION; GENETICS; GENOTYPE; HUMAN; METABOLISM; NEWBORN; PHOSPHORYLATION;

ANIMALS; ANIMALS, NEWBORN; CYCLIN-DEPENDENT KINASE 5; DOSE-RESPONSE RELATIONSHIP, DRUG; GENE EXPRESSION REGULATION, DEVELOPMENTAL; GENOTYPE; GREEN FLUORESCENT PROTEINS; HUMANS; LEAD; MICE; MICE, TRANSGENIC; MICRORNAS; PHOSPHORYLATION; RNA, MESSENGER; TAU PROTEINS;

EID: 84975463056     PISSN: 0161813X     EISSN: 18729711     Source Type: Journal    
DOI: 10.1016/j.neuro.2016.06.001     Document Type: Article

References (23)

1. Alzheimer's A. Alzheimer's disease facts and figures. Alzheimers Dement 2015, 11(3):332-384.
2. Andorfer C., Kress Y., Espinoza M., et al. Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms. J. Neurochem. 2003, 86(3):582-590. 10.1046/j.1471-4159.2003.01879.x.
3. Basha M.R., Wei W., Bakheet S.A., et al. The fetal basis of amyloidogenesis: exposure to lead and latent overexpression of amyloid precursor protein and beta-amyloid in the aging brain. J. Neurosci. 2005, 25(4):823-829. 10.1523/jneurosci.4335-04.2005.
4. Bekris L.M., Yu C.E., Bird T.D., Tsuang D.W. Genetics of Alzheimer disease. J. Geriatr. Psychiatr. Neurol. 2010, 23(4):213-227. 10.1177/0891988710383571.
5. Bihaqi S.W., Zawia N.H. Enhanced taupathy and AD-like pathology in aged primate brains decades after infantile exposure to lead (Pb). Neurotoxicology 2013, 39:95-101. 10.1016/j.neuro.2013.07.010.
6. Bihaqi S.W., Bahmani A., Adem A., Zawia N.H. Infantile postnatal exposure to lead (Pb) enhances tau expression in the cerebral cortex of aged mice: relevance to AD. Neurotoxicology 2014, 10.1016/j.neuro.2014.06.008.
7. Caillet-Boudin M.L., Buee L., Sergeant N., Lefebvre B. Regulation of human MAPT gene expression. Mol. Neurodegener. 2015, 10:28. 10.1186/s13024-015-0025-8.
8. Dosunmu R., Wu J., Basha M.R., Zawia N.H. Environmental and dietary risk factors in Alzheimer's disease. Expert Rev. Neurother. 2007, 7(7):887-900. 10.1586/14737175.7.7.887.
9. Gendron T.F., Petrucelli L. The role of tau in neurodegeneration. Mol. Neurodegener. 2009, 4:13. 10.1186/1750-1326-4-13.
10. Goodall E.F., Heath P.R., Bandmann O., Kirby J., Shaw P.J. Neuronal dark matter: the emerging role of microRNAs in neurodegeneration. Front. Cell. Neurosci. 2013, 7:178. 10.3389/fncel.2013.00178.
11. Karch C.M., Goate A.M. Alzheimer's disease risk genes and mechanisms of disease pathogenesis. Biol. Psychiatry 2014, 10.1016/j.biopsych.2014.05.006.
12. Kimura T., Ishiguro K., Hisanaga S. Physiological and pathological phosphorylation of tau by Cdk5. Front. Mol. Neurosci. 2014, 7:65. 10.3389/fnmol.2014.00065.
13. Liddell M.B., Lovestone S., Owen M.J. Genetic risk of Alzheimer's disease: advising relatives. Br. J. Psychiatry 2001, 178(1):7-11.
14. Lunnon K., Mill J. Epigenetic studies in Alzheimer's disease: current findings, caveats, and considerations for future studies. Am. J. Med. Genet. B Neuropsychiatr. Genet. 2013, 162b(8):789-799. 10.1002/ajmg.b.32201.
15. Masoud, A.M., Bihaqi S.W., Machan J.T., Zawia N.H., Renehan W.E. (2016) Early-life exposure to lead (Pb) alters the expression of microRNA that target proteins associated with Alzheimer's disease. J. Alzheimer's Dis. XX:XX.
16. Payton M., Riggs K.M., Spiro A., Weiss S.T., Hu H. Relations of bone and blood lead to cognitive function: the VA Normative Aging Study. Neurotoxicol. Teratol. 1998, 20(1):19-27.
17. Rosenthal S.L., Kamboh M.I. Late-onset Alzheimer's disease genes and the potentially implicated pathways. Curr. Genet. Med. Rep. 2014, 2:85-101. 10.1007/s40142-014-0034-x.
18. Subaiea G.M., Ahmed A.H., Adwan L.I., Zawia N.H. Reduction of amyloid-beta deposition and attenuation of memory deficits by tolfenamic acid. J. Alzheimer's Dis. JAD 2015, 43(2):425-433. 10.3233/JAD-132726.
19. Weisskopf M.G., Wright R.O., Schwartz J., et al. Cumulative lead exposure and prospective change in cognition among elderly men: the VA Normative Aging Study. Am. J. Epidemiol. 2004, 160(12):1184-1193.
20. Weisskopf M.G., Proctor S.P., Wright R.O., et al. Cumulative lead exposure and cognitive performance among elderly men. Epidemiology (Cambridge, Mass) 2007, 18(1):59-66.
21. Wright R.O., Tsaih S.W., Schwartz J., et al. Lead exposure biomarkers and mini-mental status exam scores in older men. Epidemiology (Cambridge, Mass) 2003, 14(6):713-718.
22. Wu H., Huang M., Lu M., et al. Regulation of microtubule-associated protein tau (MAPT) by miR-34c-5p determines the chemosensitivity of gastric cancer to paclitaxel. Cancer Chemother. Pharmacol. 2013, 71(5):1159-1171. 10.1007/s00280-013-2108-y.
23. Zawia N.H., Harry G.J. Developmental exposure to lead interferes with glial and neuronal differential gene expression in the rat cerebellum. Toxicol. Appl. Pharmacol. 1996, 138(1):43-47. 10.1006/taap.1996.0095.