Alzheimer's Disease Studies

The proper combination of Alzheimer’s disease in vitro assays can deliver critical information delivering insights that serve as better predictors for the transition to in vivo studies. Improve your in vivo success by integrating translational cell-based assays from simple cell proliferation and viability assays to multicellular biochemical and functional assays for high content phenotypic screening using our unique access to Alzheimer’s Disease relevant human primary cells from tissue, blood and differentiated stem cells into your AD discovery program.

APPK670/671L, has been linked to early-onset familial Alzheimer’s disease. The Tg2576 Alzheimer's Disease model overexpress this mutant form of amyloid precursor protein. Validated using multiple endpoints including cognitive testing, measurement of the levels of soluble and insoluble beta amyloid, and biomarker measurement using immunohistochemical staining at just 5 months of age.

Disruption of the cholinergic system leads to amnesia or memory loss. This Alzheimer’s animal study employs Scopolamine, a muscarinic cholinergic receptor antagonist providing a validated animal model to study impaired learning and memory in Alzheimer’s Disease research.

Our Alzheimer's Disease models include large animal models that are used to study higher cognitive function and changes. Large animal models are evaluated using a broad range cognitive test battery that is similar to the CANTAB touchscreen testing methods used in humans.

The CVN mice show statistically significant impairment compared to wild type even though the difference is not very large (10–15%). Having two CVN mice cohorts—a vehicle-treated group and a compound-treated group—would ensure that the phenotype of impaired cognition is reproduced in the vehicle-treated CVN mice. This would result in a reproducible reversal learning graph. The reversal learning (visual discrimination) resembles dimensional human touchscreen testing tasks that are commonly used to assess cognitive impairment so the similarity between rodent touchscreen testing and human touchscreen testing increases the translational index.

In CVN mice, the motor deficit is reproducible but is used more as a biomarker endpoint and less to assess efficacy. The cognitive deficit is also reproducible and is used more to assess efficacy in Alzheimer’s Disease research using fear conditioning, the Barnes maze or the radial arm water maze. Unfortunately, while the CVN mice have been used extensively, the deficit response to several neuroprotective drugs has not been very successful.

In the CVN Alzheimer’s animal model we are testing several options including treating the animals and then performing electrophysiology tests, and using compounds to study differential effects on synaptic transmission in wild-type versus diseased animals.

Large animals have been used to assess cognition using touchscreen technologies. Either aged or scopolamine-treated animals (to impair cognition) are used for touchscreen and biomarker assessment of cerebrospinal fluid (CSF).

No. One test does not have a significant benefit over the other and both tests are run routinely.

We suggest not only looking at long-term potentiation but also at the amplitude of basal synaptic transmissions. In Alzheimer’s Disease models, the basal synaptic transmission tends to get disrupted, making it easier to detect those changes compared to long-term potentiation changes.

No. In multiple blind studies, we have found similar results in small and large groups of mice.