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From genes to mechanisms to therapies: Lessons to be learned from neurological disorders

The brain is an isolated metabolic preserve and small metabolic biases that may have no consequences for other cells may have an important role in many neurological conditions.

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References

  1. Li, X.-J. et al. A huntingtin-associated protein enriched in brain with implications for pathology. Nature 378, 398–402 (1995).

    Article  CAS  Google Scholar 

  2. Burke, J.R. et al. Huntingtin and DRPLA proteins selectively interact with the enzyme GAPDH. Nature Med. 2, 347–350 (1996).

    Article  CAS  Google Scholar 

  3. Gottesman, I.I. & Bertelsen, A. Confirming unexpressed genotypes for schizophrenia. Risks in the offspring of Fischer's Danish identical and fraternal discordant twins. Arch. Gen. Psychiatry 46, 867–872 (1989).

    Article  CAS  Google Scholar 

  4. Bassett, A.S. & Honer, W.G. Evidence for anticipation in schizophrenia. Am. J. Hum. Genet. 54, 864–870 (1994).

    CAS  PubMed  PubMed Central  Google Scholar 

  5. Deng, H.X. et al. Amyotrophic lateral sclerosis and structural defects in Cu,Zn superoxide dismutase. Science 261, 1047–1051 (1993).

    Article  CAS  Google Scholar 

  6. Games, D. et al. Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein. Nature 373, 523–527 (1995).

    Article  CAS  Google Scholar 

  7. Cai, X.D., Golde, T.E. & Younkin, S.G. Release of excess amyloid beta protein from a mutant amyloid beta protein precursor. Science 259, 514–516 (1993).

    Article  CAS  Google Scholar 

  8. Sherrington, R. et al. Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature 375, 754–760 (1995).

    Article  CAS  Google Scholar 

  9. Roses, A.D., Perspective: On the metabolism of apolipoprotein E and the Alzheimer diseases. Exp. Neurol. 132, 149–156 (1995).

    Article  CAS  Google Scholar 

  10. Ueki, A., Kawano, M., Namba, Y., Kawakami, M. & Ikeda, K. A high frequency of apolipoprotein E4 isoprotein in Japanese patients with late-onset nonfamilial Alzheimer's disease. Neurosci. Lett. 163, 166–168 (1993).

    Article  CAS  Google Scholar 

  11. Kuusisto, J. et al. Association of apolipoprotein E phenotypes with late onset Alzheimer's disease: Population based study. Br. Med. J. 309, 636–638 (1994).

    Article  CAS  Google Scholar 

  12. Polvikoski, T. et al. Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein. N. Engl. J. Med. 333, 1242–1247 (1995).

    Article  CAS  Google Scholar 

  13. Ohm, T.G. et al. Apolipoprotein E polymorphism influences not only cerebral senile plaque load but also Alzheimer-type neurofibrillary tangle formation. Neuroscience 66, 583–587 (1995).

    Article  CAS  Google Scholar 

  14. Strittmatter, W.J. et al. Isoform-specific interactions of apolipoprotein E with microtubule-associated protein tau: Implications for Alzheimer disease. Proc. Natl. Acad. Sci. USA 91, 11183–11186 (1994).

    Article  CAS  Google Scholar 

  15. Nathan, B.P. et al. The inhibitory effect of apolipoprotein E4 on neurite outgrowth is associated with microtubule depolymerization. J. Biol. Chem. 270, 19791–19799 (1995).

    Article  CAS  Google Scholar 

  16. Holtzman, D.M. et al. Low density lipoprotein receptor-related protein mediates apolipoprotein E-dependent neurite outgrowth in a central nervous systemderived neuronal Cell line. Proc. Natl. Acad. Sci. USA 92, 9480–9484 (1995).

    Article  CAS  Google Scholar 

  17. Huang, D.Y. et al. Isoform-specific interactions of apolipoprotein E with the microtubule associated protein MAP2c: Implications for Alzheimer's disease. Neumsci. Lett. 182, 55–58 (1994).

    Article  CAS  Google Scholar 

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Roses, A. From genes to mechanisms to therapies: Lessons to be learned from neurological disorders. Nat Med 2, 267–269 (1996). https://doi.org/10.1038/nm0396-267

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