Parkinson's disease as a result of aging

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Abstract

It is generally considered that Parkinson's disease is induced by specific agents that degenerate a clearly defined population of dopaminergic neurons. Data commented in this review suggest that this assumption is not as clear as is often thought and that aging may be critical for Parkinson's disease. Neurons degenerating in Parkinson's disease also degenerate in normal aging, and the different agents involved in the etiology of this illness are also involved in aging. Senescence is a wider phenomenon affecting cells all over the body, whereas Parkinson's disease seems to be restricted to certain brain centers and cell populations. However, reviewed data suggest that Parkinson's disease may be a local expression of aging on cell populations which, by their characteristics (high number of synaptic terminals and mitochondria, unmyelinated axons, etc.), are highly vulnerable to the agents promoting aging. The development of new knowledge about Parkinson's disease could be accelerated if the research on aging and Parkinson's disease were planned together, and the perspective provided by gerontology gains relevance in this field.

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Most cited references 311

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Brain energy metabolism: focus on astrocyte-neuron metabolic cooperation.

Mireille Bélanger, Igor Allaman, Pierre J. Magistretti (2011)

The energy requirements of the brain are very high, and tight regulatory mechanisms operate to ensure adequate spatial and temporal delivery of energy substrates in register with neuronal activity. Astrocytes-a type of glial cell-have emerged as active players in brain energy delivery, production, utilization, and storage. Our understanding of neuroenergetics is rapidly evolving from a "neurocentric" view to a more integrated picture involving an intense cooperativity between astrocytes and neurons. This review focuses on the cellular aspects of brain energy metabolism, with a particular emphasis on the metabolic interactions between neurons and astrocytes. Copyright © 2011 Elsevier Inc. All rights reserved.

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A MicroRNA feedback circuit in midbrain dopamine neurons.

Jongpil Kim, Keiichi Inoue, Jennifer Ishii … (2007)

MicroRNAs (miRNAs) are evolutionarily conserved, 18- to 25-nucleotide, non-protein coding transcripts that posttranscriptionally regulate gene expression during development. miRNAs also occur in postmitotic cells, such as neurons in the mammalian central nervous system, but their function is less well characterized. We investigated the role of miRNAs in mammalian midbrain dopaminergic neurons (DNs). We identified a miRNA, miR-133b, that is specifically expressed in midbrain DNs and is deficient in midbrain tissue from patients with Parkinson's disease. miR-133b regulates the maturation and function of midbrain DNs within a negative feedback circuit that includes the paired-like homeodomain transcription factor Pitx3. We propose a role for this feedback circuit in the fine-tuning of dopaminergic behaviors such as locomotion.

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Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson's disease. Pathophysiologic and clinical implications.

S J Kish, K Shannak, O. Hornykiewicz (1988)

Autografting of dopamine-producing adrenal medullary tissue to the striatal region of the brain is now being attempted in patients with Parkinson's disease. Since the success of this neurosurgical approach to dopamine-replacement therapy may depend on the selection of the most appropriate subregion of the striatum for implantation, we examined the pattern and degree of dopamine loss in striatum obtained at autopsy from eight patients with idiopathic Parkinson's disease. We found that in the putamen there was a nearly complete depletion of dopamine in all subdivisions, with the greatest reduction in the caudal portions (less than 1 percent of the dopamine remaining). In the caudate nucleus, the only subdivision with severe dopamine reduction was the most dorsal rostral part (4 percent of the dopamine remaining); the other subdivisions still had substantial levels of dopamine (up to approximately 40 percent of control levels). We propose that the motor deficits that are a constant and characteristic feature of idiopathic Parkinson's disease are for the most part a consequence of dopamine loss in the putamen, and that the dopamine-related caudate deficits (in "higher" cognitive functions) are, if present, less marked or restricted to discrete functions only. We conclude that the putamen--particularly its caudal portions--may be the most appropriate site for intrastriatal application of dopamine-producing autografts in patients with idiopathic Parkinson's disease.

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Author and article information

Journal

Journal ID (nlm-ta): Aging Cell

Journal ID (iso-abbrev): Aging Cell

Journal ID (publisher-id): acel

Title: Aging Cell

Publisher: BlackWell Publishing Ltd (Oxford, UK )

ISSN (Print): 1474-9718

ISSN (Electronic): 1474-9726

Publication date (Print): June 2015

Publication date (Electronic): 09 February 2015

Volume: 14

Issue: 3

Pages: 293-308

Affiliations

[1 ]Laboratory of Neurobiology and Experimental Neurology, Department of Physiology, Faculty of Medicine, University of La Laguna La Laguna, Spain

[2 ]Center for Networked Biomedical Research in Neurodegenerative Diseases (CIBERNED) La Laguna, Spain

[3 ]Rehabilitation Service, Department of Pharmacology and Physical Medicine, Faculty of Medicine, University of La Laguna La Laguna, Spain

Author notes

Correspondence, Dr Manuel Rodríguez, Department of Physiology, Faculty of Medicine, University of La Laguna, Tenerife, 38200, Canary Islands, Spain. Tel.: +34 922 319361; fax: +34 922 319397; e-mail : mrdiaz@ 123456ull.es

Article

DOI: 10.1111/acel.12312

PMC ID: 4406659

PubMed ID: 25677794

SO-VID: c1ee599d-8f03-498d-968c-a114bab0b534

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This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Parkinson's disease as a result of aging

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Abstract

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Evolutionary Cell Biology

Most cited references 311

Brain energy metabolism: focus on astrocyte-neuron metabolic cooperation.

A MicroRNA feedback circuit in midbrain dopamine neurons.

Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson's disease. Pathophysiologic and clinical implications.

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