Alzheimer′s In A Dish ReN-GA2, Clone 3C1 NSC Line

Cells display normal karyotype as assessed by chromosome spread, STR profile and test negative for mycoplasma. Maternal blood has been screened for HIV, HTLV, Hepatitis B and C.

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Alzheimer′s in a Dish FAD ReNcell VM lines are a proprietary collection of immortalized single-cell derived clonal human neural progenitor cells that express stable levels of AD genes with multiple FAD mutations. The clonal FAD neural progenitor cells secrete different amounts of total Aþ and differ in the Aþ42/40 ratios. The clonal lines are notable in the homogeneity and relative stability of APP expression levels and pathogenic Aþ levels across multiple passages. The Alzheimer′s in a Dish collection of clonal lines allows the direct assessment of the role of Aþ42/40 ratio in regulating phospho-tau accumulations and neurofibrillary tangles pathology in AD.

Alzheimer′s In A Dish ReN-mGAP2, Clone H10 is a clonal FAD RenCell VM human neural progenitor cell line that expresses APPSL-GFP and PSEN1-mCherry.

References
Kim, et al. Amyloid-β42/40 ratio drives tau pathology in 3D human neural cell culture models of Alzheimer′s disease. Nat Commun. 2020 Mar 13;11(1):1377.
Kim, et al. A 3D human neural cell culture system for modeling Alzheimer′s disease. Nature. 2015 Jul;10(7):985-1006.
Park, et al. A 3D human triculture system modeling neurodegeneration and neuroinflammation in Alzheimer′s disease. Nat Protoc. 2015 Jul;10(7):985-1006.

Amyloid-þ (Aþ) plaques and neurofibrillary tangles are key pathological features observed in the brains of Alzheimer′s patients. Familial, early onset forms of AD (FAD) are caused by autosomal dominant inherited genetic mutations and offer an opportunity to study the effects of key mutations on the disease′s progression and pathology. To date, approximately 200 FAD mutations in amyloid þ precursor protein (APP) and/or presenilin I (PSEN1) have been reported. Recently a 3D model using genetically engineered human neural stem cells that overexpress FAD mutations was reported to recapitulate the two pathological hallmarks of AD–þ-amyloid plaques and neurofibrillary tangles. Importantly, single cell derived clonal FAD neural stem cells were used to demonstrate that high Aþ42/40 ratio and not total Aþ level directly correlated with accelerated accumulations of insoluble Aþ aggregates and pathogenic phospho-tau levels. Increased cell death was also detected in 3D-differentiated FAD clones with high Aβ42/40 ratio.

When stored at the recommended storage conditions (liquid nitrogen), ReNcell VM cells are stable up to the expiration date. Do not expose to elevated temperatures. Discard any remaining reagents after the expiration date. We recommend that the cells be used within ten passages.