Mitochondrial Ca2+ Signaling and Bioenergetics in Alzheimer’s Disease

Arnst, Nikita; Redolfi, Nelly; Lia, Annamaria; Bedetta, Martina; Greotti, Elisa; Pizzo, Paola

doi:10.3390/biomedicines10123025

Cited by 9 publications

(7 citation statements)

References 186 publications

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“…Ca 2+ flux also plays a dual role in AD progression. For instance, excessive Ca 2+ influx leads to increased ROS production and cell death due to caspase activation; however, attenuated Ca 2+ signaling may also be detrimental to ATP production ( Filadi and Greotti, 2021 ; Arnst et al, 2022 ). Modulation of MAM-resident enzymes such as ACAT1 and MAM-C99 content affects cholesterol levels and lipid homeostasis in AD, along with amyloid synthesis and synaptic transmission.…”

Section: Discussionmentioning

confidence: 99%

The contribution of mitochondria-associated endoplasmic reticulum membranes (MAMs) dysfunction in Alzheimer’s disease and the potential countermeasure

Cao

Hui

et al. 2023

Front. Neurosci.

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Alzheimer’s disease (AD) is the most common neurodegenerative disease. There are many studies targeting extracellular deposits of amyloid β-peptide (Aβ) and intracellular neurofibrillary tangles (NFTs), however, there are no effective treatments to halt the progression. Mitochondria-associated endoplasmic reticulum membranes (MAMs) have long been found to be associated with various pathogenesis hypotheses of AD, such as Aβ deposition, mitochondrial dysfunction, and calcium homeostasis. However, there is a lack of literature summarizing recent advances in the mechanism and treatment studies. Accordingly, this article reviews the latest research involving the roles of MAM structure and tethering proteins in the pathogenesis of AD and summarizes potential strategies targeting MAMs to dissect treatment perspectives for AD.

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Section: Discussionmentioning

confidence: 99%

The contribution of mitochondria-associated endoplasmic reticulum membranes (MAMs) dysfunction in Alzheimer’s disease and the potential countermeasure

Cao

Hui

et al. 2023

Front. Neurosci.

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“…Mitochondrial Ca 2+ fulfils energy requirements by regulating mitochondrial bioenergetics [32]. Typically, an increase in mitochondrial Ca 2+ is accompanied by increased respiration, NADH generation, and ATP production [33].…”

Section: Oxygen Consumption and Atp Productionmentioning

confidence: 99%

“…It should be emphasized once again, as mentioned above, that 25% of ATP production is spent only for Na + /K + -ATPase activity. It should be noted that the glutamate transporter and Na + /K + -ATPase colocalize with mitochondria and glycolytic enzymes [33]. For example, after capture by mitochondria, Ca 2+ is released back into the cytosol through the activity of Na + /Ca 2+ and H + /Ca 2+ exchangers [33].…”

Section: Atp Usementioning

confidence: 99%

Metal Toxicity: Effects on Energy Metabolism in Fish

Gashkina

2024

IJMS

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Metals are dispersed in natural environments, particularly in the aquatic environment, and accumulate, causing adverse effects on aquatic life. Moreover, chronic polymetallic water pollution is a common problem, and the biological effects of exposure to complex mixtures of metals are the most difficult to interpret. In this review, metal toxicity is examined with a focus on its impact on energy metabolism. Mechanisms regulating adenosine triphosphate (ATP) production and reactive oxygen species (ROS) emission are considered in their dual roles in the development of cytotoxicity and cytoprotection, and mitochondria may become target organelles of metal toxicity when the transmembrane potential is reduced below its phosphorylation level. One of the main consequences of metal toxicity is additional energy costs, and the metabolic load can lead to the disruption of oxidative metabolism and enhanced anaerobiosis.

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“…AD is characterized by mutations in PSEN1/2, which lead to the augmentation of the opening of mitochondrial permeability transition pore (mPTP) Ca 2+ -releasing channels, producing an extreme statement of Ca 2+ from this store [92,93]. The accumulation of Ca 2+ in the mitochondria usually leads to cell death compelled via necrosis and apoptosis [94]. Moreover, mitochondrial Ca 2+ excess can impair mitochondria via mitophagy.…”

Section: Ca 2+ Ions In the Regulation Of Mitophagymentioning

confidence: 99%

The Role of Mitochondrial Dysfunction in Alzheimer’s: Molecular Defects and Mitophagy-Enhancing Approaches

Farsi

2023

Life

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Alzheimer’s disease (AD), a progressive and chronic neurodegenerative syndrome, is categorized by cognitive and memory damage caused by the aggregations of abnormal proteins, specifically including Tau proteins and β-amyloid in brain tissue. Moreover, mitochondrial dysfunctions are the principal causes of AD, which is associated with mitophagy impairment. Investigations exploring pharmacological therapies alongside AD have explicitly concentrated on molecules accomplished in preventing/abolishing the gatherings of the abovementioned proteins and mitochondria damages. Mitophagy is the removal of dead mitochondria by the autophagy process. Damages in mitophagy, the manner of diversified mitochondrial degeneracy by autophagy resulting in an ongoing aggregation of malfunctioning mitochondria, were also suggested to support AD. Recently, plentiful reports have suggested a link between defective mitophagy and AD. This treaty highlights updated outlines of modern innovations and developments on mitophagy machinery dysfunctions in AD brains. Moreover, therapeutic and nanotherapeutic strategies targeting mitochondrial dysfunction are also presented in this review. Based on the significant role of diminished mitophagy in AD, we suggest that the application of different therapeutic approaches aimed at stimulating mitophagy in AD would be beneficial for targeting or reducing the mitochondrial dysfunction induced by AD.

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Mitochondrial Ca2+ Signaling and Bioenergetics in Alzheimer’s Disease

Cited by 9 publications

References 186 publications

The contribution of mitochondria-associated endoplasmic reticulum membranes (MAMs) dysfunction in Alzheimer’s disease and the potential countermeasure

The contribution of mitochondria-associated endoplasmic reticulum membranes (MAMs) dysfunction in Alzheimer’s disease and the potential countermeasure

Metal Toxicity: Effects on Energy Metabolism in Fish

The Role of Mitochondrial Dysfunction in Alzheimer’s: Molecular Defects and Mitophagy-Enhancing Approaches

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