Synapse loss is one of the common factors contributing to
cognitive disorders, such as
Alzheimer's disease (AD), which is manifested by the impairment of basic cognitive functions including memory processing, perception, problem solving, and language. The current
therapies for patients with
cognitive disorders are mainly palliative; thus, regimens preventing and/or delaying
dementia progression are urgently needed. In this study, we evaluated the effects of
catalpol, isolated from
traditional Chinese medicine Rehmannia glutinosa, on synaptic plasticity in aged rat models. We found that
catalpol markedly improved the cognitive function of aged male Sprague-Dawley rats and simultaneously increased the expression of synaptic
proteins (
dynamin 1, PSD-95, and
synaptophysin) in the cerebral cortex and hippocampus, respectively. In
beta-amyloid (Aβ) injured primary rat's cortical neuron,
catalpol did not increase the viability of neuron but extended the length of
microtubule-associated protein 2 (MAP-2) positive neurites and reversed the suppressive effects on expression of synaptic
proteins induced by Aβ. Additionally, the effects of
catalpol on stimulating the growth of MAP-2 positive neurites and the expression of synaptic
proteins were diminished by a PKC inhibitor,
bisindolylmaleimide I, suggesting that PKC may be implicated in
catalpol's function of preventing the neurodegeneration induced by Aβ. Altogether, our study indicates that
catalpol could be a potential disease-modifying drug for
cognitive disorders such as AD.