Abstract
Alzheimer’s disease (AD) is the most common progressive neurodegenerative disease. Today, AD affects millions of people worldwide and the number of AD cases will further increase with longer life expectancy. The AD brain is marked by severe neurodegeneration, such as the loss of synapses and neurons, atrophy and depletion of neurotransmitter systems, especially in the hippocampus and cerebral cortex. Recent findings highlight the important role of mitochondrial dysfunction and increased oxidative stress in the pathophysiology of late-onset alzheimer’s disease (LOAD). These alterations are not only observed in the brain of AD patients but also in the periphery. In this review, we discuss the potential role of elevated apoptosis, increased oxidative stress and mitochondrial dysfunction as peripheral markers for the detection of AD in blood cells e.g. lymphocytes. We evaluate recent findings regarding impaired mitochondrial function comprising mitochondrial respiration, reduced complex activities of the respiratory chain and altered Mitochondrial Membrane Potential (MMP) in lymphocytes as well as in neurons. Finally, we will question whether these mitochondrial parameters might be suitable as an early peripheral marker for the detection of LOAD but also for the transitional stage between normal aging and Dementia, “Mild Cognitive Impairment” (MCI).
Keywords: Alzheimers disease, neurodegeneration, mitochondria, lymphocytes, brain, mitochondrial dysfunction, ROS, genetics.
Current Alzheimer Research
Title:Mitochondrial Dysfunction as a Causative Factor in Alzheimer’s Disease-Spectrum Disorders: Lymphocytes as a Window to the Brain
Volume: 18 Issue: 10
Author(s): Marko Jörg, Johanna E. Plehn, Kristina Friedland and Walter E. Müller*
Affiliation:
- Department of Pharmacology, Biocenter, Goethe University, Frankfurt,Germany
Keywords: Alzheimers disease, neurodegeneration, mitochondria, lymphocytes, brain, mitochondrial dysfunction, ROS, genetics.
Abstract: Alzheimer’s disease (AD) is the most common progressive neurodegenerative disease. Today, AD affects millions of people worldwide and the number of AD cases will further increase with longer life expectancy. The AD brain is marked by severe neurodegeneration, such as the loss of synapses and neurons, atrophy and depletion of neurotransmitter systems, especially in the hippocampus and cerebral cortex. Recent findings highlight the important role of mitochondrial dysfunction and increased oxidative stress in the pathophysiology of late-onset alzheimer’s disease (LOAD). These alterations are not only observed in the brain of AD patients but also in the periphery. In this review, we discuss the potential role of elevated apoptosis, increased oxidative stress and mitochondrial dysfunction as peripheral markers for the detection of AD in blood cells e.g. lymphocytes. We evaluate recent findings regarding impaired mitochondrial function comprising mitochondrial respiration, reduced complex activities of the respiratory chain and altered Mitochondrial Membrane Potential (MMP) in lymphocytes as well as in neurons. Finally, we will question whether these mitochondrial parameters might be suitable as an early peripheral marker for the detection of LOAD but also for the transitional stage between normal aging and Dementia, “Mild Cognitive Impairment” (MCI).
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Cite this article as:
Jörg Marko, Plehn E. Johanna, Friedland Kristina and Müller E. Walter *, Mitochondrial Dysfunction as a Causative Factor in Alzheimer’s Disease-Spectrum Disorders: Lymphocytes as a Window to the Brain, Current Alzheimer Research 2021; 18 (10) . https://dx.doi.org/10.2174/1567205018666211208141512
DOI https://dx.doi.org/10.2174/1567205018666211208141512 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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