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[Engadin]

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P A Y W A L L E D   S O U R C E :   Mechanisms of Aging and Development

 

 

 

 

 

 

Highlights

 

 

  •  Transcription factors, cytoplasmic regulators and OMM proteins are essential for mitochondrial biogenesis.

 

  •  The abundance of mitochondrial biogenesis regulators and mitochondria is altered during ageing.

 

  •  Mild elevation in mitochondrial biogenesis has an anti-ageing role.

 

  •  Mild elevation in mitochondrial biogenesis is neuroprotective.

 

  •  Impaired mitochondrial biogenesis and function trigger AD, PD and HD onset and progression

 

 

 

Abstract

 

Mitochondrial biogenesis is indispensable for organismal homeostasis. The semi-autonomous nature of mitochondria makes their biogenesis rather complex, as it requires the contribution of the nucleus, the cytoplasm and the organelle itself. Recently, several transcription regulators, RNA binding proteins and outer mitochondrial membrane (OMM) components have been implicated in the regulation of the process.

 

Both the expression and the abundance of several of these factors are altered during ageing, and their impairment can have diverse, yet principally detrimental, effects on lifespan. These findings converge on the notion that mitochondrial biogenesis is an age-modulated process that, when perturbed, compromises survival.

 

Notably, core brain functions are dependent on mitochondrial metabolite availability. Indeed, emerging evidence indicates that mitochondrial biogenesis regulators play important roles in the onset and progression of severe neurodegenerative syndromes such as AD, PD and HD.

 

These devastating human pathologies remain incurable to date. A better understanding of the mechanisms that govern mitochondrial biogenesis could facilitate the development of effective pharmaceutical interventions against these diseases.

 

 

 

Outline

 

1. Introduction

 

2. Mitochondrial biogenesis regulators

  2.1. Nuclear regulators

      2.1.1. Nuclear respiratory factors

      2.1.2. Nuclear factor erythroid 2-related factor 2 (Nrf2)

      2.1.3. Nuclear Hormone receptors

      2.1.4. CREB

      2.1.5. Proliferator-activated receptor γ coactivator-1

  2.2. Cytoplasmic regulators

  2.3. OMM regulators

 

3. Mitochondrial biogenesis and organismal senescence

 

4. Mitochondrial biogenesis and neurodegeneration

  4.1. Alzheimer's disease

  4.2. Parkinson's disease

  4.3. Huntington's disease

 

5. Conclusions and future prospects

 

 

 

 

 

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[OlderThanThou2]

Cocoa beans improve mitochondrial biogenesis via PPARγ/PGC1α dependent signalling pathway in MPP + intoxicated human neuroblastoma cells (SH-SY5Y)

https://pubmed.ncbi....h.gov/30207204/

 

Interesting, cocoa increases mitochondria fusion:

 

 

Abstract

Polyphenols are shown to protect from or delay the progression of chronic neurodegenerative diseases. Mitochondrial dysfunction plays a key role in the pathogenesis of Parkinson's disease (PD). This study was aims to gain insight into the role of ahydroalcoholic extract of cocoa (standardised for epicatechin content) on mitochondrial biogenesis in MPP+ intoxicated human neuroblastoma cells (SHSY5Y). The effects of cocoa on PPARγ, PGC1α, Nrf2 and TFAM protein expression and mitochondrial membrane potential were evaluated. A pre-exposure to cocoa extract decreased reactive oxygen species formation and restored mitochondrial membrane potential. The cocoa extract was found to up-regulate the expression of PPARγ and the downstream signalling proteins PGC1α, Nrf2 and TFAM. It increased the expression of the anti-apoptotic protein BCl2 and increased superoxide dismutase activity. Further, the cocoa extract down-regulated the expression of mitochondria fission 1 (Fis1) and up-regulated the expression of mitochondria fusion 2 (Mfn2) proteins, suggesting an improvement in mitochondrial functions in MPP+ intoxicated cells upon treatment with cocoa. Interestingly, cocoa up-regulates the expression of tyrosine hydroxylase, the rate limiting enzyme in dopamine synthesis. No change in the expression of PPARγ on treatment with cocoa extract was observed when the cells were pre-treated with PPARγ antagonist GW9662. This data suggests that cocoa mediates mitochondrial biogenesis via a PPARγ/PGC1α dependent signalling pathway and also has the ability to improve dopaminergic functions by increasing tyrosine hydroxylase expression. Based on our data, we propose that a cocoa bean extract and products thereof could be used as potential nutritional supplements for neuroprotection in PD.

 

 

Might be the stearic acid in it.

Edited by OlderThanThou2, 03 September 2020 - 03:57 PM.