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Stem Cell Res. 2019 Jan;34:101370. doi: 10.1016/j.scr.2018.101370. Epub 2018 Dec 19.

Derivation of iPSC lines from two patients with familial Alzheimer's disease from India.

Author information

1
National Centre for Biological Sciences (NCBS), Tata Institute of Fundamental Research (TIFR), Bengaluru, India; Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, India.
2
Institute for Stem Cell Biology and Regenerative Medicine (InStem), Bengaluru, India.
3
National Institute of Mental Health and Neurosciences (NIMHANS), Bengaluru, India.
4
Department of Toxicology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, India.
5
National Centre for Biological Sciences (NCBS), Tata Institute of Fundamental Research (TIFR), Bengaluru, India; Department of Physiology and Biophysics, School of Medicine, University of California, Irvine, USA.
6
National Centre for Biological Sciences (NCBS), Tata Institute of Fundamental Research (TIFR), Bengaluru, India; Institute for Stem Cell Biology and Regenerative Medicine (InStem), Bengaluru, India. Electronic address: omukherjee@ncbs.res.in.
7
National Centre for Biological Sciences (NCBS), Tata Institute of Fundamental Research (TIFR), Bengaluru, India; National Institute of Mental Health and Neurosciences (NIMHANS), Bengaluru, India. Electronic address: sjain.nimhans@nic.in.

Abstract

The current prevalence of diagnosable dementia in India is 1% of people over 60 years (~3.7 million people), but is estimated to increase significantly, as ~15% world's aged population (>65 years) would be resident here by 2020 (Shah et al., 2016). While several mutations that pose a familial risk have been identified, the ethnic background may influence disease susceptibility, clinical presentation and treatment response. In this study, we report a detailed characterization of two representative HiPSC lines from a well-characterized dementia cohort from India. Availability of these lines, and associated molecular and clinical information, would be useful in the detailed exploration of the genomic contribution(s) to AD.

PMID:
30605839
DOI:
10.1016/j.scr.2018.101370
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