Differential Role of Active Compounds in Mitophagy and Related Neurodegenerative Diseases

Makarov, Mark; Korkotian, Eduard

doi:10.3390/toxins15030202

Cited by 6 publications

(4 citation statements)

References 177 publications

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“…When mitochondrial autophagy is impaired, these crucial functions of mitochondria are affected, disrupting calcium ion homeostasis and the mitochondrial respiratory chain. This can induce mutations in mitochondrial DNA, leading to cell degeneration, apoptosis, and the onset or exacerbation of neurodegenerative diseases (Makarov & Korkotian, 2023; Simone et al., 2020).…”

Section: Role Of Mitophagy In Maintaining Synaptic Plasticity and Lea...mentioning

confidence: 99%

Advancements in the study of synaptic plasticity and mitochondrial autophagy relationship

Zhu,

Hui,

Zhang

et al. 2024

J of Neuroscience Research

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Synapses serve as the points of communication between neurons, consisting primarily of three components: the presynaptic membrane, synaptic cleft, and postsynaptic membrane. They transmit signals through the release and reception of neurotransmitters. Synaptic plasticity, the ability of synapses to undergo structural and functional changes, is influenced by proteins such as growth‐associated proteins, synaptic vesicle proteins, postsynaptic density proteins, and neurotrophic growth factors. Furthermore, maintaining synaptic plasticity consumes more than half of the brain's energy, with a significant portion of this energy originating from ATP generated through mitochondrial energy metabolism. Consequently, the quantity, distribution, transport, and function of mitochondria impact the stability of brain energy metabolism, thereby participating in the regulation of fundamental processes in synaptic plasticity, including neuronal differentiation, neurite outgrowth, synapse formation, and neurotransmitter release. This article provides a comprehensive overview of the proteins associated with presynaptic plasticity, postsynaptic plasticity, and common factors between the two, as well as the relationship between mitochondrial energy metabolism and synaptic plasticity.

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Section: Role Of Mitophagy In Maintaining Synaptic Plasticity and Lea...mentioning

confidence: 99%

Advancements in the study of synaptic plasticity and mitochondrial autophagy relationship

Zhu,

Hui,

Zhang

et al. 2024

J of Neuroscience Research

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“…These diverse functions encompass the modulation of calcium homeostasis, mitochondrial function, autophagy, and mitophagy. The hypothesis suggests a relative primacy of mitochondrial dysfunction over amyloid accumulation in the pathogenesis of AD and is currently subject to debate (Makarov and Korkotian, 2023). While the deleterious effects of amyloid accumulation are well-established, the question arises as to whether a single amyloid accumulation event is sufficient to elicit subsequent pathological consequences, and whether the amyloid hypothesis is excessively emphasized.…”

Section: The Mitochondrial Cascade Hypothesismentioning

confidence: 99%

Presenilins and mitochondria—an intriguing link: mini-review

et al. 2023

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This review uncovers the intricate relationship between presenilins, calcium, and mitochondria in the context of Alzheimer’s disease (AD), with a particular focus on the involvement of presenilin mutations in mitochondrial dysfunction. So far, it is unclear whether the impairment of mitochondrial function arises primarily from damage inflicted by β-amyloid upon mitochondria or from the disruption of calcium homeostasis due to presenilins dysfunctions. The roles of presenilins in mitophagy, autophagy, mitochondrial dynamics, and many other functions, non-γ-secretase related, also require close attention in future research. Resolution of contradictions in understanding of presenilins cellular functions are needed for new effective therapeutic strategies for AD.

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“…As noticed, spermidine was able to rescue the mitochondrial function of SH-SY5Y cells expressing a mutant form of the human tau protein (P301L tau mutation) [ 260 ]. As an autophagy inducer, spermidine modulates the mTOR and AMPK pathways [ 261 ] and activates Ataxia Telangiectasia mutated (ATM)-dependent PINK1/Parkin signaling [ 262 ].…”

Section: Mitochondria-based Therapies For Alzheimer’s Diseasementioning

confidence: 99%

Current Advances in Mitochondrial Targeted Interventions in Alzheimer’s Disease

Sousa,

Moreira,

Cardoso

2023

Biomedicines

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Alzheimer’s disease is the most prevalent neurodegenerative disorder and affects the lives not only of those who are diagnosed but also of their caregivers. Despite the enormous social, economic and political burden, AD remains a disease without an effective treatment and with several failed attempts to modify the disease course. The fact that AD clinical diagnosis is most often performed at a stage at which the underlying pathological events are in an advanced and conceivably irremediable state strongly hampers treatment attempts. This raises the awareness of the need to identify and characterize the early brain changes in AD, in order to identify possible novel therapeutic targets to circumvent AD’s cascade of events. One of the most auspicious targets is mitochondria, powerful organelles found in nearly all cells of the body. A vast body of literature has shown that mitochondria from AD patients and model organisms of the disease differ from their non-AD counterparts. In view of this evidence, preserving and/or restoring mitochondria’s health and function can represent the primary means to achieve advances to tackle AD. In this review, we will briefly assess and summarize the previous and latest evidence of mitochondria dysfunction in AD. A particular focus will be given to the recent updates and advances in the strategy options aimed to target faulty mitochondria in AD.

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Differential Role of Active Compounds in Mitophagy and Related Neurodegenerative Diseases

Cited by 6 publications

References 177 publications

Advancements in the study of synaptic plasticity and mitochondrial autophagy relationship

Advancements in the study of synaptic plasticity and mitochondrial autophagy relationship

Presenilins and mitochondria—an intriguing link: mini-review

Current Advances in Mitochondrial Targeted Interventions in Alzheimer’s Disease

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