In vivo brain imaging of mitochondrial Ca2+ in neurodegenerative diseases with multiphoton microscopy

Calvo-Rodríguez, María; Kharitonova, Elizabeth K.; Bacskai, Brian J.

doi:10.1016/j.bbamcr.2021.118998

Cited by 12 publications

(8 citation statements)

References 200 publications

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“…This leads to mitochondrial dysfunction, the generation of ROS, and the activation of apoptosis (Figure 1). Mitochondrial dysfunction in AD is an important pathogenesis pathway and includes mitochondrial oxidative stress, disruption of cellular bioenergetics, and the induction of neuronal apoptosis [29].…”

Section: Mitochondriamentioning

confidence: 99%

The Role of Oxygen Homeostasis and the HIF-1 Factor in the Development of Neurodegeneration

Mitroshina,

Vedunova

2024

IJMS

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Understanding the molecular underpinnings of neurodegeneration processes is a pressing challenge for medicine and neurobiology. Alzheimer’s disease (AD) and Parkinson’s disease (PD) represent the most prevalent forms of neurodegeneration. To date, a substantial body of experimental evidence has strongly implicated hypoxia in the pathogenesis of numerous neurological disorders, including AD, PD, and other age-related neurodegenerative conditions. Hypoxia-inducible factor (HIF) is a transcription factor that triggers a cell survival program in conditions of oxygen deprivation. The involvement of HIF-1α in neurodegenerative processes presents a complex and sometimes contradictory picture. This review aims to elucidate the current understanding of the interplay between hypoxia and the development of AD and PD, assess the involvement of HIF-1 in their pathogenesis, and summarize promising therapeutic approaches centered on modulating the activity of the HIF-1 complex.

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Section: Mitochondriamentioning

confidence: 99%

The Role of Oxygen Homeostasis and the HIF-1 Factor in the Development of Neurodegeneration

Mitroshina,

Vedunova

2024

IJMS

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“…For example, in Alzheimer's disease (AD), elevated Ca 2+ flux from the ER to the mitochondria was observed along with increased MAM formation and elevated levels of IP3Rs and VDAC1, which were all linked to an increased level of amyloid β (Aβ) [136][137][138]. The excessive mitochondrial Ca 2+ loading was also observed in the neurons of living brain by performing multiphoton microscopy via a cranial window on mouse models for AD [139]. Interestingly, several MAM proteins, such as PACS-2 and S1R, were also found to be upregulated at the MAMs in both AD mouse models and AD patient cells, thereby modulating the IP3R-GRP75-VDAC1 complex [137].…”

Section: The Ip3r-grp75-vdac1 Complex In Patho(physio)logical Situationsmentioning

confidence: 99%

The ER-mitochondria interface, where Ca2+ and cell death meet

et al. 2023

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“…It has become more and more clear that mitochondria play a fundamental role in the pathophysiology of AD ( Figure 4 ) [ 107 ]. More specifically, mitochondrial dysfunction has been reported as an early event in AD, as it precedes the onset of plaque formation in the 3xTg-AD mouse model [ 108 ].…”

Section: Alzheimer’s Diseasementioning

confidence: 99%

Dysregulated Ca2+ Homeostasis as a Central Theme in Neurodegeneration: Lessons from Alzheimer’s Disease and Wolfram Syndrome

Callens

Loncke

Bultynck

2022

Cells

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Calcium ions (Ca2+) operate as important messengers in the cell, indispensable for signaling the underlying numerous cellular processes in all of the cell types in the human body. In neurons, Ca2+ signaling is crucial for regulating synaptic transmission and for the processes of learning and memory formation. Hence, the dysregulation of intracellular Ca2+ homeostasis results in a broad range of disorders, including cancer and neurodegeneration. A major source for intracellular Ca2+ is the endoplasmic reticulum (ER), which has close contacts with other organelles, including mitochondria. In this review, we focus on the emerging role of Ca2+ signaling at the ER–mitochondrial interface in two different neurodegenerative diseases, namely Alzheimer’s disease and Wolfram syndrome. Both of these diseases share some common hallmarks in the early stages, including alterations in the ER and mitochondrial Ca2+ handling, mitochondrial dysfunction and increased Reactive oxygen species (ROS) production. This indicates that similar mechanisms may underly these two disease pathologies and suggests that both research topics might benefit from complementary research.

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In vivo brain imaging of mitochondrial Ca2+ in neurodegenerative diseases with multiphoton microscopy

Cited by 12 publications

References 200 publications

The Role of Oxygen Homeostasis and the HIF-1 Factor in the Development of Neurodegeneration

The Role of Oxygen Homeostasis and the HIF-1 Factor in the Development of Neurodegeneration

The ER-mitochondria interface, where Ca2+ and cell death meet

Dysregulated Ca2+ Homeostasis as a Central Theme in Neurodegeneration: Lessons from Alzheimer’s Disease and Wolfram Syndrome

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