The information of Beta Amyloid [25-35] Peptide

Fragment of Beta Amyloid [25-35] Peptide  , functionally required for the neurotrophic and neurotoxic effects associated with Alzheimer's disease.Beta Amyloid [25-35] Peptide may cause malfunction and death of neurons in Alzheimer’s disease. We investigated the effect of Aβ on key transporters of amino acid neurotransmission in cells cultured from rat cerebral cortex. The cultures were treated with Beta Amyloid [25-35] Peptide  at 3 and 10 μM for 12 and 24 h followed by quantitative analysis of immunofluorescence intensity.

The results indicate that Beta Amyloid [25-35] Peptide  may impair neuronal function and transmitter synthesis, and perhaps reduce excitotoxicity, through a reduction in neuronal glutamine uptake. In mixed neuronal–glial cell cultures (from P1 rats), Aβ reduced the concentration of system A glutamine transporter 1 (SAT1), by up to 50% expressed relative to the neuronal marker microtubule-associated protein 2 (MAP2) in the same cell. No significant effects were detected on vesicular glutamate transporters VGLUT1 or VGLUT2 in neurons, or on glial system N glutamine transporter 1 (SN1). In neuronal cell cultures (from E18 rats), Beta Amyloid [25-35] Peptide  did not reduce SAT1 immunoreactivity, suggesting that the observed effect depends on the presence of astroglia.
Read more:Beta Amyloid [25-35] Peptide  price