Human Synthetic Amyloid Beta 1-42 Pre-formed Fibrils

Applications: ELISA

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Reactive species: Human

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"Abstract: Background: Alzheimer's disease (AD) involves cognitive decline, amyloid-beta (Aβ) accumulation, tau hyperphosphorylation, and neuroinflammation. CREB1, a key transcription factor for memory, is downregulated in AD, contributing to disease progression. Phosphodiesterases 4 and 10 (PDE4 and PDE10) are key enzymes that degrade cAMP, a second messenger involved in CREB signaling, synaptic plasticity, and neuroprotection. Dysregulation of PDE activity has been implicated in AD and other neurodegenerative disorders. Methods: We used human iPSC-derived cortical neurons and microglia, along with the APP/PS1 mouse model, to investigate the role of CREB1 and assess the therapeutic potential of dual PDE4/10A inhibition in AD. Results: CREB1 deficiency in neurons increased Aβ and p-tau231 accumulation. Dual inhibition of PDE4 and PDE10A activated the cAMP-PKA-CREB pathway, restoring CREB1 activity, reducing Aβ and p-tau231, and mitigating neuroinflammation. This intervention improved synaptic plasticity and cognitive performance in vivo. Conclusions: Our findings demonstrate that dual PDE4/10A inhibition synergistically enhances the cAMP-PKA-CREB signaling, promoting neuroprotection and synaptic remodeling. This approach offers a promising therapeutic strategy for modifying AD pathology and restoring cognitive function."

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Article snippet: Human iPSC-derived microglia were treated with preformed synthetic Human Synthetic Amyloid Beta 1–42 Pre-formed Fibrils (5 μM, CD creative diagnostics, PFF12) for 48 h to model amyloid exposure.