Mitochondrial damage-induced abnormal glucose metabolism with ageing in the hippocampus of APP/PS1 mice

Li, Shijie; Wang, Yangyang; Zhang, Xiong; Xiong, Xiaomin; Zhou, Fanlin; Li, Xiaoju; Fan, Jianing; Liang, Xiao; Li, Guangxin; Peng, Yan; Yu, Lei

doi:10.1007/s11306-023-02023-9

Cited by 3 publications

(1 citation statement)

References 53 publications

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“…Increased basal and coupled respiration in the hippocampus along with a decreased Complex II-dependent respiratory activity were observed in TgCRND8 female mice [120]. APP/PS1 transgenic mice, the AD animal model we described in the previous section, showed increased cognitive impairment, hippocampal neuron mitochondrial damage, and autophagosome accumulation with aging [121]. The 5 × FAD mouse models had a significant decrease in ATP levels in the hippocampus [122] and decreased complex I, III, and IV with increased complex V relative to wild-type mice by mitochondrial proteomic analysis [123].…”

Section: Mitochondria Dysfunction In Alzheimer's Diseasementioning

confidence: 81%

Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease

Wu,

Hsieh

2023

Antioxidants

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Bioenergetic mitochondrial dysfunction is a common feature of several diseases, including Alzheimer’s disease (AD), where redox imbalance also plays an important role in terms of disease development. AD is an age-related disease and begins many years before the appearance of neurodegenerative symptoms. Intracellular tau aggregation, extracellular β-amyloid (Aβ) deposition in the brain, and even the APOE4 genotype contribute to the process of AD by impairing redox homeostasis and mitochondrial dysfunction. This review summarizes the evidence for the redox imbalance and mitochondrial dysfunction in AD and demonstrates the current therapeutic strategies related to mitochondrial maintenance.

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Section: Mitochondria Dysfunction In Alzheimer's Diseasementioning

confidence: 81%

Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease

Wu,

Hsieh

2023

Antioxidants

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Miro-mediated mitochondrial transport: A new dimension for disease-related abnormal cell metabolism?

Li,

Yang,

Zhang

et al. 2024

Biochemical and Biophysical Research Communications

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Tricarboxylic Acid Cycle Intermediates and Individual Ageing

Kurhaluk

2024

Biomolecules

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Anti-ageing biology and medicine programmes are a focus of genetics, molecular biology, immunology, endocrinology, nutrition, and therapy. This paper discusses metabolic therapies aimed at prolonging longevity and/or health. Individual components of these effects are postulated to be related to the energy supply by tricarboxylic acid (TCA) cycle intermediates and free radical production processes. This article presents several theories of ageing and clinical descriptions of the top markers of ageing, which define ageing in different categories; additionally, their interactions with age-related changes and diseases related to α-ketoglutarate (AKG) and succinate SC formation and metabolism in pathological states are explained. This review describes convincingly the differences in the mitochondrial characteristics of energy metabolism in animals, with different levels (high and low) of physiological reactivity of functional systems related to the state of different regulatory systems providing oxygen-dependent processes. Much attention is given to the crucial role of AKG and SC in the energy metabolism in cells related to amino acid synthesis, epigenetic regulation, cell stemness, and differentiation, as well as metabolism associated with the development of pathological conditions and, in particular, cancer cells. Another goal was to address the issue of ageing in terms of individual characteristics related to physiological reactivity. This review also demonstrated the role of the Krebs cycle as a key component of cellular energy and ageing, which is closely associated with the development of various age-related pathologies, such as cancer, type 2 diabetes, and cardiovascular or neurodegenerative diseases where the mTOR pathway plays a key role. This article provides postulates of postischaemic phenomena in an ageing organism and demonstrates the dependence of accelerated ageing and age-related pathology on the levels of AKG and SC in studies on different species (roundworm Caenorhabditis elegans, Drosophila, mice, and humans used as models). The findings suggest that this approach may also be useful to show that Krebs cycle metabolites may be involved in age-related abnormalities of the mitochondrial metabolism and may thus induce epigenetic reprogramming that contributes to the senile phenotype and degenerative diseases. The metabolism of these compounds is particularly important when considering ageing mechanisms connected with different levels of initial physiological reactivity and able to initiate individual programmed ageing, depending on the intensity of oxygen consumption, metabolic peculiarities, and behavioural reactions.

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Mitochondrial damage-induced abnormal glucose metabolism with ageing in the hippocampus of APP/PS1 mice

Cited by 3 publications

References 53 publications

Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease

Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer’s Disease

Miro-mediated mitochondrial transport: A new dimension for disease-related abnormal cell metabolism?

Tricarboxylic Acid Cycle Intermediates and Individual Ageing

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