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Alzheimer's disease (AD) is the most common form of neurodegenerative disease, characterized by two aberrant features, the amyloid plaques and the neurofibrillary tangles. The initial pathophysiologic changes of AD are found in the hippocampus region of the brain, disrupting memory and the ability to learn. AD progression is linked to nerve cell dysfunction and cell death due to the accumulation of two protein aggregates: β-amyloid (Aβ) and tau. This cognitive and memory decline age-related disease causes suffering to the patient and their caregivers. Getting treatment or prevention of AD has attracted extensive attention worldwide. As a result, scientists are putting great efforts in understanding the mechanisms underlying the development of the disease as well as treatment for the disease.
The well-known neuropathogenic hallmarks of AD consist of aggregated amyloid beta (Aβ) and abnormal neurites. It is demonstrated that a dysregulated proteolytic processing of its precursor molecule, the Amyloid Precursor Protein (APP), can cause the accumulation of Aβ. Aβ can also cause caspases-mediated tau cleavage and hyperphosphorylation by activating specific kinases, thus promoting its aggregation, mis-localization and accumulation with consequent neurofibrillary tangles formation. On the other hand, Tau is a neuron specific microtubule-associated protein that regulates microtubule stability, tau dissociates from microtubules and forms insoluble aggregates called neurofibrillary tangles (NFTs). Both total tau (t-tau) and phosphorylated tau (p-tau) proteins are measured and associated with AD. Thus, Aβ peptide and tau exert crucial roles in neuronal loss or dysfunction, which would cause the increased reactive oxygen species (ROS) production, membrane damage, altered mitochondrial metabolism, abortive cell cycle events, and DNA damage/repair and inflammatory processes inevitably leading to neuronal dysfunction. Based on the above understanding, an appropriate in vitro model is deeply needed to mimic the pathogenesis and progression of AD, which could also work better with assays to study the drug candidates for Alzheimer's disease.
With extensive experience and state-of-the-art technologies, Creative Bioarray is offering Alzheimer's diseases modeling and assays to help our customers open the door for generating new insight into disease pathophysiology and improving the process of drug development.
Disease Modeling and assays available
Creative Bioarray offers development of custom designed in vitro models by using primary neuronal cultures, cell lines, iPS cells with genetic modifications, which are phenotypically closer to the adult neuronal network and mimic the development of AD. Our custom model services focus on but not restricted to AD induced by the accumulation and aggregation of Aβ. We also offer a wide range of assays that enable more accurate prediction of patient response to pharmacotherapy:
We provide this powerful and versatile tool for AD therapy as well as basic research to help our customers understand more about the underlying mechanisms in the progression of AD.
Figure 1. Neurite outgrowth is inhibited by (intracellular) amyloid and tau treatment, and rescued by β-secretase inhibitor and methylene blue respectively.
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