Cell experiment:

Primary cortical neurons are preincubated either alone (positive control) or with three concentrations of Neuropeptide Y (29-64), amide, human (TFA) (NPY) (0.5, 1, and 2 μM) for 24 h and then exposed to Aβ25-35 (50 μM) or Aβ35-25 (50 μM) for 48 h[1].

Neuropeptide Y (29-64), amide, human (TFA) is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity.

It is showed that Neuropeptide Y (29-64), amide, human (TFA) is able to protect cortical neurons from Aβ25-35 toxicity. 2 μM NPY abolishes the toxic effects of Aβ25-35 at 24 and 48 h. The same effect on neuronal survival is observed in neurons exposed to 1 μM and 0.5 μM Neuropeptide Y (29-64), amide, human (TFA) pretreatments. Pretreatment with Neuropeptide Y (29-64), amide, human (TFA) Increases NGF Synthesis, reduces NGF mRNA, and restores NGF release in cortical neurons exposed to Aβ35-25[1].

[1]. Croce N, et al. Neuropeptide Y protects rat cortical neurons against β-amyloid toxicity and re-establishes synthesis and release of nerve growth factor. ACS Chem Neurosci. 2012 Apr 18;3(4):312-8.