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P4‐284: Efficient Introduction of Disease‐Related Mutations Into Human Ipscs Using CRISPR/CAS9 to Model Alzheimer’s Disease
Author(s) -
Kwart Dylan,
Paquet Dominik,
Chen Antonia,
Sproul Andrew,
Jacob Samson,
Teo Shaun,
Olsen Kimberly Moore,
Gregg Andrew,
Noggle Scott,
Tessier-Lavigne Marc
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.07.026
Subject(s) - crispr , genome editing , cas9 , biology , indel , genetics , computational biology , induced pluripotent stem cell , gene , gene knockin , mutation , point mutation , homology directed repair , dna repair , nucleotide excision repair , genotype , single nucleotide polymorphism , embryonic stem cell
values in these networks (Fig. 2). Within the homotopic connectivity, long and short intrahemispheric and heterotopic connectivity, there were significant FCFS differences between groups (Fig. 3(A, B)). Finally, we observed significant negative correlations between the FCFS values and MMSE in default mode network and long intrahemispheric connectivity group, and between the FCFS values andMoCA in the long intrahemispheric connectivity group (P< 0.05, corrected) (Fig. 4). Conclusions:The disruption of brain dynamic functional connectivity networks in AD continuum could be revealed by resting-state fNIRS. These findings highlight the potential of FCFS of resting-state fNIRS as the sensitive biomarker for AD.