Cited by 145Alzheimer's disease research and treatmentsMitochondrial Function and PathologyAutophagy in Disease and Therapy

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Alzheimer’s disease and type 2 diabetes-related alterations in brain mitochondria, autophagy and synaptic markers

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Carvalho, Cristina, Santos, Maria S., Oliveira, Catarina R., Moreira, Paula I.·2015·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

DOI 10.1016/j.bbadis.2015.05.001

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Abstract

We aimed to investigate mitochondrial function, biogenesis and autophagy in the brain of type 2 diabetes (T2D) and Alzheimer's disease (AD) mice. Isolated brain mitochondria and homogenates from cerebral cortex and hippocampus of wild-type (WT), triple transgenic AD (3xTg-AD) and T2D mice were used to evaluate mitochondrial functional parameters and protein levels of mitochondrial biogenesis, autophagy and synaptic integrity markers, respectively. A significant decrease in mitochondrial respiration, membrane potential and energy levels was observed in T2D and 3xTg-AD mice. Also, a significant decrease in the levels of autophagy-related protein 7 (ATG7) and glycosylated lysosomal membrane protein 1 (LAMP1) was observed in cerebral cortex and hippocampus of T2D and 3xTg-AD mice. Moreover, both brain regions of 3xTg-AD mice present lower levels of nuclear respiratory factor (NRF) 1 while the levels of NRF2 are lower in both brain regions of T2D and 3xTg-AD mice. A decrease in mitochondrial encoded, nicotinamide adenine dinucleotide dehydrogenase subunit 1 (ND1) was also observed in T2D and 3xTg-AD mice although only statistically significant in T2D cortex. Furthermore, a decrease in the levels of postsynaptic density protein 95 (PSD95) in the cerebral cortex of 3xTg-AD mice and in hippocampus of T2D and 3xTg-AD mice and a decrease in the levels of synaptosomal-associated protein 25 (SNAP 25) in the hippocampus of T2D and 3xTg-AD mice were observed suggesting synaptic integrity loss. These results support the idea that alterations in mitochondrial function, biogenesis and autophagy cause synaptic damage in AD and T2D.

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Authors: Carvalho, C., Santos, M. S., Oliveira, C. R., & Moreira, P. I.
Affiliations: Centro de Neurociências e Biologia Celular (PT)
University of Coimbra (PT)
Corresponding author: Carvalho, Cristina
Moreira, Paula I.
ORCID: Carvalho, Cristina
Santos, Maria S.
Oliveira, Catarina R.
Moreira, Paula I.
Venue: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher: Elsevier BV
Published: 2015-08
Volume: 1852
Issue: 8
Pages: 1665-1675
ISSN: 0925-4439 (ISSN-L)
DOI: 10.1016/j.bbadis.2015.05.001
OpenAlex: W285963485
Cited by: 145
References: 79
Citations by year: 2026: 3 · 2025: 11 · 2024: 15 · 2023: 11 · 2022: 15 · 2021: 18 · 2020: 22 · 2019: 15 · 2018: 9 · 2017: 12 · 2016: 11 · 2015: 3
FWCI: 8.60
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 366 d)
Locations: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
PubMed (publishedVersion)
Funders: Quadro de Referência Estratégico Nacional (13853 QREN DO-IT)
Foundation for Science and Technology (04539)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords: Alzheimer's disease, type 2 diabetes, brain mitochondria, mitochondrial biogenesis, autophagy, synaptic integrity, mitochondrial respiration, mitochondrial membrane potential, ATG7, LAMP1, NRF1, Nrf2, ND1, PSD-95, SNAP-25, 3xTg-AD mice, cerebral cortex, hippocampus
MeSH terms: Alzheimer Disease, Animals, Autophagy, Brain, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Disease Models, Animal, Male, Mice, Transgenic, Mitochondria, Synapses, Biomarkers, Mice

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Alzheimer’s disease and type 2 diabetes-related alterations in brain mitochondria, autophagy and synaptic markers

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