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Interactions with and Membrane Permeabilization of Brain Mitochondria by Amyloid Fibrils
Published on: September 28, 2019
Effect of β-amyloid (25-35) on mitochondrial function and expression of mitochondrial permeability transition pore
Rui Ren1, Yang Zhang, Benchang Li
1Toxicology Group, Public Health College, Harbin Medical University, Harbin, PR China.
Abstract:
The aim of this study was to assess the effect of the β-amyloid fragment Aβ(25-35) on mitochondrial structure and function and on the expression of proteins associated with the mitochondrial permeability transition pore (MPTP) in rat hippocampal neurons. Ninety clean-grade Sprague-Dawley rats were randomly assigned to six groups (n = 15 per group). Aβ(25-35) (1, 5, or 10 µg/rat) was injected into hippocampal area CA1. Normal saline was injected as a control. The effect of Aβ(25-35) injection on hippocampal structure was assessed by transmission electron microscopy. Ca(2+) -ATPase activity, [Ca(2+) ](i) , and mitochondrial membrane potential were measured. The expression of genes associated with the MPTP, including the voltage-dependent anion channel (VDAC), adenine nucleotide translocator (ANT), and cyclophilin D (Cyp-D), were evaluated. Results showed that Aβ(25-35) injection damaged the mitochondrial structure of hippocampal neurons, decreased Ca(2+) -ATPase activity and mitochondrial membrane potential, and increased [Ca(2+) ](i) . The expression levels for VDAC, ANT, and Cyp-D in all groups were significantly (P < 0.05) higher than those in the normal control group after Aβ(25-35) injection. These results indicate that Aβ(25-35) damages mitochondria in rat hippocampal neurons and effects mitochondrial dysfunction, as well as increasing the expression of genes associated with the MPTP. Mitochondrial dysfunction may result in increased MPTP gene expression, leading to neurodegenerative effects.
Insights
Beta-amyloid (Aβ(25-35)) fragment damages rat hippocampal neuron mitochondria, impairing function and increasing mitochondrial permeability transition pore (MPTP) gene expression. This suggests a link between mitochondrial dysfunction and neurodegeneration.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Beta-amyloid fragments are implicated in neurodegenerative diseases.
- Mitochondrial dysfunction is a key factor in neuronal cell death.
- The mitochondrial permeability transition pore (MPTP) plays a role in apoptosis.
Purpose of the Study:
- To investigate the impact of the beta-amyloid fragment Aβ(25-35) on mitochondrial structure and function.
- To examine the effect of Aβ(25-35) on the expression of MPTP-associated proteins in rat hippocampal neurons.
Main Methods:
- Rats received injections of Aβ(25-35) or saline into the hippocampal CA1 region.
- Transmission electron microscopy assessed mitochondrial structure.
- Mitochondrial function was evaluated by measuring Ca(2+)-ATPase activity, intracellular calcium ([Ca(2+)](i)), and mitochondrial membrane potential.
- Gene expression of VDAC, ANT, and Cyp-D (MPTP components) was analyzed.
Main Results:
- Aβ(25-35) induced damage to mitochondrial structure in hippocampal neurons.
- Mitochondrial function was impaired, evidenced by decreased Ca(2+)-ATPase activity and membrane potential, and increased [Ca(2+)](i).
- Expression of VDAC, ANT, and Cyp-D genes was significantly elevated post-Aβ(25-35) injection.
Conclusions:
- Aβ(25-35) causes mitochondrial damage and dysfunction in rat hippocampal neurons.
- Increased expression of MPTP-associated genes suggests a role in Aβ-induced neurotoxicity.
- Mitochondrial dysfunction and MPTP activation may contribute to neurodegenerative processes.
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