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Exogenous fibroblast growth factor 1 ameliorates diabetes-induced cognitive decline via coordinately regulating
Yanqing Wu1,2, Chengbiao Wu3, Libing Ye2
1The Institute of Life Sciences, Engineering Laboratory of Zhejiang province for pharmaceutical development of growth factors, Biomedical Collaborative Innovation Center of Wenzhou, Wenzhou University, Wenzhou, 325035, China.
Background:
Diabetes induces central nervous system damage, leading to cognitive decline. Fibroblast growth factor 1 (FGF1) has dual function of neuroprotection and normalizing hyperglycemia. To date, the precise mechanisms and potential treating strategies of FGF1 for diabetes-induced cognitive decline (DICD) hasn't been fully elucidated.
Methods:
In this study, db/db mice were used as DICD animal model. We found that diabetes remarkably suppressed FGF1 expression in hippocampus. Thus, exogenous FGF1 had been treated for db/db mice and SH-SY5Y cells.
Results:
FGF1 significantly ameliorates DICD with better spatial learning and memory function. Moreover, FGF1 blocked diabetes-induced morphological structure change, neuronal apoptosis and Aβ1-42 deposition and synaptic dysfunction in hippocampus. But normalizing glucose may not the only contributed factor for FGF1 treating DICD with evidencing that metformin-treated db/db mice has a inferior cognitive function than that in FGF1 group. Current mechanistic study had found that diabetes inhibits cAMP-response element binding protein (CREB) activity and subsequently suppresses brain derived neurotrophic factor (BDNF) level via coordinately regulating PERK signaling and PI3K/AKT signaling in hippocampus, which were reversed by FGF1.
Conclusion:
We conclude that FGF1 exerts its neuroprotective role and normalizing hyperglycemia effect, consequently ameliorates DICD, implying FGF1 holds a great promise to develop a new treatment for DICD. Video abstract.
Insights
Fibroblast growth factor 1 (FGF1) protects against diabetes-induced cognitive decline by preserving brain structure and function. FGF1 offers a promising therapeutic strategy for this condition, beyond just glucose control.
Area of Science:
- Neuroscience
- Endocrinology
- Pharmacology
Background:
- Diabetes mellitus is a significant risk factor for central nervous system damage, manifesting as cognitive decline.
- Fibroblast growth factor 1 (FGF1) exhibits neuroprotective properties and the ability to normalize hyperglycemia.
- The exact mechanisms by which FGF1 combats diabetes-induced cognitive decline (DICD) remain incompletely understood.
Purpose of the Study:
- To investigate the therapeutic potential of FGF1 in an animal model of diabetes-induced cognitive decline (DICD).
- To elucidate the underlying molecular mechanisms through which FGF1 exerts its neuroprotective effects in the context of diabetes.
Main Methods:
- Utilized db/db mice as a model for DICD and SH-SY5Y cells for in vitro studies.
- Administered exogenous FGF1 to diabetic mice and assessed cognitive functions, including spatial learning and memory.
- Examined hippocampal tissue for structural changes, neuronal apoptosis, amyloid-beta deposition, and synaptic function.
Main Results:
- FGF1 treatment significantly improved cognitive function in diabetic mice.
- FGF1 administration prevented diabetes-associated neuronal damage, apoptosis, amyloid-beta deposition, and synaptic dysfunction in the hippocampus.
- FGF1's efficacy in improving cognitive function surpassed that of metformin, suggesting mechanisms beyond glucose normalization.
- FGF1 reversed diabetes-induced inhibition of CREB activity and BDNF levels by modulating PERK and PI3K/AKT signaling pathways.
Conclusions:
- FGF1 demonstrates significant neuroprotective effects and hyperglycemia-normalizing capabilities, effectively ameliorating diabetes-induced cognitive decline (DICD).
- FGF1 presents a promising therapeutic candidate for the development of novel treatments for DICD.
- The study highlights FGF1's multifaceted action involving key signaling pathways crucial for neuronal health and function.
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