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Clinical progression in Parkinson disease and the neurobiology of axons
Open accessAbstract
Despite tremendous growth in recent years in our knowledge of the molecular basis of Parkinson disease (PD) and the molecular pathways of cell injury and death, we remain without therapies that forestall disease progression. Although there are many possible explanations for this lack of success, one is that experimental therapeutics to date have not adequately focused on an important component of the disease process, that of axon degeneration. It remains unknown what neuronal compartment, either the soma or the axon, is involved at disease onset, although some have proposed that it is the axons and their terminals that take the initial brunt of injury. Nevertheless, this concept has not been formally incorporated into many of the current theories of disease pathogenesis, and it has not achieved a wide consensus. More importantly, in view of growing evidence that the molecular mechanisms of axon degeneration are separate and distinct from the canonical pathways of programmed cell death that mediate soma destruction, the possibility of early involvement of axons in PD has not been adequately emphasized as a rationale to explore the neurobiology of axons for novel therapeutic targets. We propose that ongoing degeneration of axons, not cell bodies, is the primary determinant of clinically apparent progression of disease, and that future experimental therapeutics intended to forestall disease progression will benefit from a new focus on the distinct mechanisms of axon degeneration.
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“The diagnosis of PD is reliant on clinical motor symptoms and neuroimaging; however, by the onset of symptoms, it is estimated that 50–70% of substantia nigra pars compacta dopaminergic neurons have already been lost [247, 248].”
From Extracellular vesicles as nanotheranostic platforms for targeted neurological disorder interventions (2024) · cites this paper as [247]
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“PD patients can expect to lose up 60-80% of all dopaminergic neurons throughout PD progression leading to the depletion of dopamine within the brain (Cheng et al., 2010).”
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Erythropoietin as a Modulator of Pathology in a Toxicant Mouse Model of Parkinson’s Disease
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Muddapu, V. R., Vijayakumar, K., Ramakrishnan, K., & Chakravarthy, V. S. (2020) · arXiv (Cornell University) · doi:10.48550/arxiv.2004.08320 · Cited by 1
“From both homogeneous and heterogeneous energy deficiency results, it suggests that SNc (axonal) terminals are more vulnerable to energy imbalance when compared to SNc cell bodies (somas) which was observed experimentally, where injury is initiated at axonal terminals (Burré et al., 2010; Cheng et al., 2010; Giguère e…”
BackgroundOkuda, S., Uemura, N., Sawamura, M., Taguchi, T., Ikuno, M., Uemura, M. T., Yamakado, H., & Takahashi, R. (2021) · Research Square · doi:10.21203/rs.3.rs-355605/v1 · Cited by 1
Bureau, S. C. (2022) · Carleton University's Institutional Repository (MacOdrum Library, Carleton University) · doi:10.22215/etd/2022-14889 · Cited by 1
Stillman, N. H., Joseph, J. A., Ahmed, J., Dohoney, R. A., Ball, T. D., Thomas, A. G., Fitch, T. C., Donnelly, C. M., & Kumar, S. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.07.11.499659 · Cited by 1
Radlicka-Borysewska, A., Jabłońska, J., Lenarczyk, M., Szumiec, Ł., Harda, Z., Bagińska, M., Pera, J., Kreiner, G., Wojcik, D. K., & Parkitna, J. M. R. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.01.23.525182 · Cited by 1
Naaldijk, Y., Fernández, B., Fasiczka, R., Fdez, E., Leghay, C., Croitoru, I. M., Kwok, J. B., Boulesnane, Y., Vizeneux, A., Mutez, E., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.04.11.536367 · Cited by 1
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Theologidis, V., Ferreira, S. A., Jensen, N. M., Moreira, D. G., Ahlgreen, O. A., Hansen, M. W., Rosenberg, E. D., Richner, M., Faress, I. M. G., Gram, H., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.09.05.610956 · Cited by 1
Bioenergetic signature of Synaptic mitochondriaPreprint
Faria‐Pereira, A., & Morais, V. A. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.11.28.625855 · Cited by 1
Impaired glymphatic clearance independently contributes to poor outcomes in Parkinson’s diseasePreprint
Zarkali, A., Thomas, G. E. C., Paterson, R. W., Hannaway, N., Dobreva, I., Heslegrave, A., Veleva, E., Zetterberg, H., & Weil, R. S. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.01.15.633106 · Cited by 1
Maladies des noyaux de la base
Cambier, J., Masson, M., Masson, C., & Dehen, H. (2012) · Elsevier eBooks · doi:10.1016/b978-2-294-71451-1.00013-3
Microdevices for Isolating Single Axons for the Study of Axonal Transport in Dopaminergic Neurons
Lu, X. (2013) · Open Scholarship Institutional Repository (Washington University in St. Louis) · doi:10.7936/k7ft8j1n
Fusion Models and “Fusioning” in Parkinsonism: Protection and Restoration by Exercise
Archer, T., & Fredriksson, A. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_95
The Neuroprotective Potential of STN DBS and the Role of BDNF
Fischer, D. L. (2015) · Michigan State University Libraries · doi:10.25335/m5s778
Evidence of oligodendrogliosis in MPTP-induced Parkinsonism 1
Annese, V., Barcia, C., Ros‐Bernal, F., Bernárdez-Gómez, A., Ros, C. M. B., de Pablos, V., Stefano, M. E. D., Herrero, M. T., & Darwin, C. R. (2012)
Lessons learned: neuroprotective trials in Parkinson's disease
Beaulieu‐Boire, I., & Lang, A. E. (2016) · Cambridge University Press eBooks · doi:10.1017/cbo9781107284210.025
Hacker, M. L., & Charles, D. P. (2016) · Cambridge University Press eBooks · doi:10.1017/cbo9781107284210.029
Clinical Trials in Parkinson's Diease: Lessons, Controversies and Challenges
(2016) · Cambridge University Press eBooks · doi:10.1017/cbo9781107284210.022
Cell surface GRP78 and its interactions with CDNF and MANF
de Almeida, S. F. (2016) · Työväentutkimus Vuosikirja
Anxiety and depression in Parkinson’s disease
Broen, M. P. G. (2016) · Research Publications (Maastricht University) · doi:10.26481/dis.20161202mb
Mirfakhrai, F., Mohammadi, Z. F., & mohammadi, H. F. (2017) · Zahedan Journal of Research in Medical Sciences · doi:10.5812/zjrms.8954
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Clinical role of a subcortical communication
Pelzer, E. A. (2016) · Journal of Neurology and Neuromedicine · doi:10.29245/2572.942x/2016/5.1041
GDNF and Neurturin isoforms in an experimental model of Parkinson's disease
Penttinen, A. (2017) · Työväentutkimus Vuosikirja
Parent, K. L. (2017) · UA Campus Repository (The University of Arizona)
Longitudinal magnetic resonance imaging of cognitive impairment in Parkinson’s disease
Almuqbel, M. M. (2018) · Otago University Research Archive (University of Otago)
Efficacy of Rhythmic Acquisition on Gait Performance Among Individuals with Parkinson’s Disease
Kogutek, D. (2018) · Scholarship@Western (Western University)
Neuromechanical Simulation of Hand Pronation and Supination Task in Parkinson’s disease
Ziegelmanl, L., Hu, Y., & Hernandez, M. E. (2018) · Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) · doi:10.1109/embc.2018.8512605
“70 of the normal input to no input as Parkinsonian symptoms first appear when 30 percent of substancia nigra neurons are lost [12].”
BackgroundClinical Prediction Rules for Using Aerobic Exercises on Executive Functions in Parkinson's Patients
Shehata, F., Elwishy, A., Kishk, N. A., & Ahmed, G. M. (2018) · Journal of Medical Sciences(Faisalabad) · doi:10.3923/jms.2018.157.163
Novel methods for biological network inference: an application to circadian Ca2+ signaling network
Jin, J. (2018) · Apollo (University of Cambridge) · doi:10.17863/cam.32695
In memoriam: Robert E. Burke, MD, 1949–2018
Fahn, S., Sulzer, D. L., Kang, U. J., & Bressman, S. (2019) · Movement Disorders · doi:10.1002/mds.27612
WITHDRAWN: Genetics of Parkinson’s disease
Lill, C. M. (2020) · Molecular and Cellular Probes · doi:10.1016/j.mcp.2019.101471
Retracted
Metadata
- Authors
- Cheng, H., Ulane, C. M., & Burke, R. E.
- Affiliations
- Columbia University Irving Medical Center (US)
- Corresponding author
- Burke, Robert E.
- ORCID
- Burke, Robert E.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2010-05-26
- Volume
- 67
- Issue
- 6
- Pages
- 715-725
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC2918373
- OpenAlex
- W1967659552
- Cited by
- 1,012
- References
- 77
- Citations by year
- 2026: 56 · 2025: 74 · 2024: 101 · 2023: 92 · 2022: 108 · 2021: 109 · 2020: 100 · 2019: 82 · 2018: 67 · 2017: 59 · 2016: 35 · 2015: 36 · 2014: 24 · 2013: 22 · 2012: 23
- FWCI
- 12.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS26836, P50NS038370, R56NS026836, NS38370, R01NS026836)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Keywords
- Parkinson's disease, axonal degeneration, disease progression, axonal injury, programmed cell death, therapeutic target, pathogenesis, axon terminals
- MeSH terms
- Axons, Humans, Neurobiology, Neurons, Parkinson Disease, Disease Progression
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