Alzheimer's disease is one of the most economically and socially impactful diseases of our time. Through basic and clinical research, top genes that are mutated in Alzheimer's disease have been identified. However, it is complex and challenging to select the right mutants to study due to too many choices of strains and alleles (genetic models). In addition, researchers sometimes have doubts that a strain obtained from another source has not lost the mutation or undergone genetic drift. Our goal is to create a curated, reliable library of strains that are relevant to Alzheimer's disease. We have carefully selected: These sequence validated strains enable researchers to: 
Alzheimer’s Disease Panel
Preselected disease-relevant strains that are sequence validated.
| Strain | Human Gene | Worm Gene Homologue | Type of transgenic | Protein activity | Worm Phenotype |
|---|---|---|---|---|---|
| ALZ PSEN1 Knock-out1 | PSEN1 - 70% of all early onset Alzheimer’s | sel-12 | Loss of Function. Improper processing of APP protein | Plaque formation | Egg laying defect |
| ALZ Humanized Aβ2 | Aβ (cleavage product of APP) | N/A | Gain on Function. Human disease gene expressed in worm | Plaque formation | Paralysis |
| ALZ Humanized MAPT3 | MAPT | ptl-1 | Gain of Function Addition of humanized disease gene | tau tangles | Uncoordinated |
Key advantages of the Alzheimer’s Panel
- Ready-to-screen format (Fig. 1) enables quicker identification of drug impacts
- Genetic mutations are validated with sequencing
- Recommended reference strains selected for their relevance to Alzheimer’s disease
- Consistent number of animals received
- 3 different packaging to choose from
- Vial (frozen)
- Petri plate (room temperature)
- 96-well plate (room temperature)
Fig 1. Day-2 ALZ PSEN1 Knock-out live C. elegans on NGM plate. This worm was dyed with both RediStain™ WormDyes Lyso (magenta) and Neuro Green (cyan) to stain sensory neurons and apoptotic corpses in the gonad respectively. The sel-12(ty11) mutation produces defects in vulva and neuronal development leading to a dysfunctional uterine-vulval connection and ultimately the inability to lay eggs. The worm is positioned head-down on the left and head-up on the right.
Video: Day-1 adult ALZ Humanized MAPT C. elegans in 5HT 10mM. This worm immobilized into a ScreenChip Channel expresses GFP in the pharyngeal muscles under the control of the myo-2 promoter.
Ordering information
| Strain | Qty | Format | Cat. No. | Price |
|---|---|---|---|---|
| ALZ PSEN1 Knock-out | 1 | Vial Petri plate 96-well plate |
ALZ-001 | $350.00 |
| ALZ Aβ - humanized | 1 | Vial Petri plate 96-well plate |
ALZ-002 | $350.00 |
| ALZ Humanized MAPT | 1 s | Vial Petri plate 96-well plate |
ALZ-002 | $350.00 |
References
- Levitan D et al. Assessment of normal and mutant human presenilin function in Caenorhabditis elegans. Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14940-4. https://www.ncbi.nlm.nih.gov/pubmed/8962160
- McColl G et al. Utility of an improved model of amyloid-beta (Aβ₁₋₄₂) toxicity in Caenorhabditis elegans for drug screening for Alzheimer's disease. Mol Neurodegener. 2012 Nov 21;7:57. doi: 10.1186/1750-1326-7-57. https://www.ncbi.nlm.nih.gov/pubmed/23171715
- Kraemer BC et al. Neurodegeneration and defective neurotransmission in a Caenorhabditis elegans model of tauopathy. Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9980-5. Epub 2003 Jul 18. https://www.ncbi.nlm.nih.gov/pubmed/12872001