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Mitochondrial Dysfunction Contributes to the Pathogenesis of Alzheimer's Disease.

Cabezas-Opazo FA, Vergara-Pulgar K, Pérez MJ, Jara C, Osorio-Fuentealba C, Quintanilla RA - Oxid Med Cell Longev (2015)

Bottom Line: Currently, there is no effective treatment for AD, which indicates the necessity to understand the pathogenic mechanism of this disorder.Mitochondria are essential for brain cells function and the improvement of mitochondrial activity contributes to preventing neurodegeneration.These defects affect mitochondrial health, which later will contribute to the pathogenesis of AD.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile, San Miguel, 8900000 Santiago, Chile.

ABSTRACT
Alzheimer's disease (AD) is a neurodegenerative disease that affects millions of people worldwide. Currently, there is no effective treatment for AD, which indicates the necessity to understand the pathogenic mechanism of this disorder. Extracellular aggregates of amyloid precursor protein (APP), called Aβ peptide and neurofibrillary tangles (NFTs), formed by tau protein in the hyperphosphorylated form are considered the hallmarks of AD. Accumulative evidence suggests that tau pathology and Aβ affect neuronal cells compromising energy supply, antioxidant response, and synaptic activity. In this context, it has been showed that mitochondrial function could be affected by the presence of tau pathology and Aβ in AD. Mitochondria are essential for brain cells function and the improvement of mitochondrial activity contributes to preventing neurodegeneration. Several reports have suggested that mitochondria could be affected in terms of morphology, bioenergetics, and transport in AD. These defects affect mitochondrial health, which later will contribute to the pathogenesis of AD. In this review, we will discuss evidence that supports the importance of mitochondrial injury in the pathogenesis of AD and how studying these mechanisms could lead us to suggest new targets for diagnostic and therapeutic intervention against neurodegeneration.

No MeSH data available.


Related in: MedlinePlus

Mitochondrial dysfunction in AD. Factors that contributed to AD such as injury, aging, and inflammation can affect three critical aspects of mitochondrial function: (1) mitochondrial dynamics (inducing fragmentation), (2) bioenergetics (ATP and ROS production), and (3) mitochondrial movement (synaptic function). ATP: adenosine triphosphate; ΔΨ: mitochondrial membrane potential; ROS: reactive oxygen species.
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Related In: Results  -  Collection


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fig1: Mitochondrial dysfunction in AD. Factors that contributed to AD such as injury, aging, and inflammation can affect three critical aspects of mitochondrial function: (1) mitochondrial dynamics (inducing fragmentation), (2) bioenergetics (ATP and ROS production), and (3) mitochondrial movement (synaptic function). ATP: adenosine triphosphate; ΔΨ: mitochondrial membrane potential; ROS: reactive oxygen species.

Mentions: Defects in mitochondrial transport regularly affect neuronal function including autophagy and neuronal communication and finally could induce synaptic loss [11–13]. These effects have been observed in different cellular and mice models used to replicate AD pathology [11–13] and represent an important factor in the progression of AD. In this review, we will discuss evidence in which mitochondrial transport impairment is contributing to neurodegeneration in AD.


Mitochondrial Dysfunction Contributes to the Pathogenesis of Alzheimer's Disease.

Cabezas-Opazo FA, Vergara-Pulgar K, Pérez MJ, Jara C, Osorio-Fuentealba C, Quintanilla RA - Oxid Med Cell Longev (2015)

Mitochondrial dysfunction in AD. Factors that contributed to AD such as injury, aging, and inflammation can affect three critical aspects of mitochondrial function: (1) mitochondrial dynamics (inducing fragmentation), (2) bioenergetics (ATP and ROS production), and (3) mitochondrial movement (synaptic function). ATP: adenosine triphosphate; ΔΨ: mitochondrial membrane potential; ROS: reactive oxygen species.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4499633&req=5

fig1: Mitochondrial dysfunction in AD. Factors that contributed to AD such as injury, aging, and inflammation can affect three critical aspects of mitochondrial function: (1) mitochondrial dynamics (inducing fragmentation), (2) bioenergetics (ATP and ROS production), and (3) mitochondrial movement (synaptic function). ATP: adenosine triphosphate; ΔΨ: mitochondrial membrane potential; ROS: reactive oxygen species.
Mentions: Defects in mitochondrial transport regularly affect neuronal function including autophagy and neuronal communication and finally could induce synaptic loss [11–13]. These effects have been observed in different cellular and mice models used to replicate AD pathology [11–13] and represent an important factor in the progression of AD. In this review, we will discuss evidence in which mitochondrial transport impairment is contributing to neurodegeneration in AD.

Bottom Line: Currently, there is no effective treatment for AD, which indicates the necessity to understand the pathogenic mechanism of this disorder.Mitochondria are essential for brain cells function and the improvement of mitochondrial activity contributes to preventing neurodegeneration.These defects affect mitochondrial health, which later will contribute to the pathogenesis of AD.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile, San Miguel, 8900000 Santiago, Chile.

ABSTRACT
Alzheimer's disease (AD) is a neurodegenerative disease that affects millions of people worldwide. Currently, there is no effective treatment for AD, which indicates the necessity to understand the pathogenic mechanism of this disorder. Extracellular aggregates of amyloid precursor protein (APP), called Aβ peptide and neurofibrillary tangles (NFTs), formed by tau protein in the hyperphosphorylated form are considered the hallmarks of AD. Accumulative evidence suggests that tau pathology and Aβ affect neuronal cells compromising energy supply, antioxidant response, and synaptic activity. In this context, it has been showed that mitochondrial function could be affected by the presence of tau pathology and Aβ in AD. Mitochondria are essential for brain cells function and the improvement of mitochondrial activity contributes to preventing neurodegeneration. Several reports have suggested that mitochondria could be affected in terms of morphology, bioenergetics, and transport in AD. These defects affect mitochondrial health, which later will contribute to the pathogenesis of AD. In this review, we will discuss evidence that supports the importance of mitochondrial injury in the pathogenesis of AD and how studying these mechanisms could lead us to suggest new targets for diagnostic and therapeutic intervention against neurodegeneration.

No MeSH data available.


Related in: MedlinePlus