Ex Vivo Assays
- Brain and brain substructures
- Crude extracts
- Subcellular fractioning
- Synaptosomal preparations
- Membranes and lipid rafts preparations
- Cerebrospinal fluid
- Blood, plasma
- Peripheral tissues
Biochemistry / Immunochemistry investigating:
- Synaptic markers (e.g. SNAP25, PSD 95, synaptophysin, synaptotagmin)
- Inflammation markers (e.g. IL1β, TNFα, IL6, ...)
- Cell signaling (e.g. MAPkinase, STAT3, PI3k/Akt, CREB, …)
- Oxidative stress (e.g. ROS, 4HNE, GSH, …)
- Amyloid loads (soluble & fibrillar)
- Lipids and fatty acids
SynAging has established the loss of synaptic markers and neuroinflammation in its phenotypic mouse model of Alzheimer’ Disease, which is induced by a single icv injection of its highly reproducible amyloid-β or tau oligomers.
Following behavioral evaluation, SynAging is now offering validated routine quantitative ELISA assays of important pre- and post-synaptic marker proteins:
SNAP25, PSD95, and synaptophysin are reduced significantly in AβO or hTO treated mice and restored by the neuroprotective peptide humanin, validated in multiple independent experiments.To SynAging's knowledge, loss of synaptic markers has not been shown for any other Alzheimer model on the market so far.
Furthermore, induction of TNFα, IL1β and IL6 are reproducibly seen after treatment of primary astrocytes with misfolded protein aggregates. More information is shown in SynAging's Alzheimer in vitro AbO model presentation.The changes of neuroinflammatory markers have also been valuated in the AbO induced mouse in vivo:
SynAging’s AbO induce impairment of cell signaling (reduced actin phosphorylation, P-Act, compared to total actin, Act) and synaptic function (reduced presence of: glutamate receptor 2 and 3, GluR2/3) in primary neurons and protection by humanin peptide (HNG).