Correlation between depression, physical exercise and neurodegenerative diseases
DOI:
https://doi.org/10.12775/QS.2024.16.002Keywords
Depression, Neurodegeneration, physical exercise, Huntington's disease, Parkinson's disease, Alzheimer’s diseaseAbstract
Introduction:
Depression is the most common mental disorder, affecting a significant percentage of the adult population. The disease is associated with many negative health consequences and is one of the leading causes of disability and inability to work worldwide. This neurological condition is commonly associated with neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). In recent decades, advancements have uncovered certain pathophysiological and molecular mechanisms underlying these disorders. These revelations suggest that, although they exhibit unique characteristics, there are notable parallels in the neurobiological changes associated with major depressive disorder (MDD) and the neurodegenerative processes in Alzheimer's disease, Parkinson's disease, and Huntington's disease. In this article the relevance of non-pharmacological therapies in the management of neurodegenerative diseases have been rising. Almost absent from side effects, non-pharmacological alternatives, including physical exercise have shown promising benefits.
Aim of the study:
The study aims to evaluate the association between depression symptoms and neurodegenerative diseases. Moreover, we indicate sport as a way to preserve and improve cognitive function, and to maintain a proper quality of life.
Material and methods:
We conducted a review of scientific publications published in the years 1998-2024 in English and Polish in the PubMed and Google Scholar databases. We used keywords such as "depression", "neurodegeneration” and “physical exercise”.
Conclusions:
Depression has been demonstrated to be a risk factor for neurodegenerative diseases and suggested to be a possible prodrome for them. However, sport can alleviate behavioral symptoms in neurodevelopmental disorders, like anxiety, depression, indifference and sleep disruptions.
References
M. Hussain, P. Kumar, S. Khan, D. K. Gordon, and S. Khan, “Similarities Between Depression and Neurodegenerative Diseases: Pathophysiology, Challenges in Diagnosis and Treatment Options,” Cureus, Nov. 2020, doi: 10.7759/cureus.11613.
Z. Hu et al., “Prospective Role of MicroRNAs in Depression,” Current Medicinal Chemistry, vol. 24, no. 32, pp. 3508–3521.
R. Ding et al., “The role of microRNAs in depression,” Front. Pharmacol., vol. 14, Mar. 2023, doi: 10.3389/fphar.2023.1129186.
I. M. Goodyer, J. Herbert, A. Tamplin, and P. M. E. Altham, “Recent life events, cortisol, dehydroepiandrosterone and the onset of major depression in high-risk adolescents,” Br J Psychiatry, vol. 177, no. 6, pp. 499–504, Dec. 2000, doi: 10.1192/bjp.177.6.499.
J. Keller et al., “HPA axis in major depression: cortisol, clinical symptomatology and genetic variation predict cognition,” Mol Psychiatry, vol. 22, no. 4, pp. 527–536, Apr. 2017, doi: 10.1038/mp.2016.120.
F. S. Dafsari and F. Jessen, “Depression—an underrecognized target for prevention of dementia in Alzheimer’s disease,” Transl Psychiatry, vol. 10, no. 1, p. 160, May 2020, doi: 10.1038/s41398-020-0839-1.
I. Marques-Aleixo et al., “Preventive and Therapeutic Potential of Physical Exercise in Neurodegenerative Diseases,” Antioxidants & Redox Signaling, vol. 34, no. 8, pp. 674–693, Mar. 2021, doi: 10.1089/ars.2020.8075.
N. Tsuno and A. Homma, “What is the association between depression and Alzheimer’s disease?,” Expert Review of Neurotherapeutics, vol. 9, no. 11, pp. 1667–1676, Nov. 2009, doi: 10.1586/ern.09.106.
S. Wuwongse, R. C.-C. Chang, and A. C. K. Law, “The putative neurodegenerative links between depression and Alzheimer’s disease,” Progress in Neurobiology, vol. 91, no. 4, pp. 362–375, Aug. 2010, doi: 10.1016/j.pneurobio.2010.04.005.
J. Carter and C. Lippa, “β-Amyloid, Neuronal Death and Alzheimers Disease,” CMM, vol. 1, no. 6, pp. 733–737, Dec. 2001, doi: 10.2174/1566524013363177.
J. K. Young, “Neurogenesis Makes a Crucial Contribution to the Neuropathology of Alzheimer’s Disease,” ADR, vol. 4, no. 1, pp. 365–371, Sep. 2020, doi: 10.3233/ADR-200218.
N. Uchida et al., “Glutamate-stimulated proliferation of rat retinal pigment epithelial cells,” European Journal of Pharmacology, vol. 343, no. 2–3, pp. 265–273, Feb. 1998, doi: 10.1016/S0014-2999(97)01526-4.
J. L. Cummings, “Alzheimer’s Disease,” N Engl J Med, vol. 351, no. 1, pp. 56–67, Jul. 2004, doi: 10.1056/NEJMra040223.
A. Abeliovich et al., “Mice Lacking α-Synuclein Display Functional Deficits in the Nigrostriatal Dopamine System,” Neuron, vol. 25, no. 1, pp. 239–252, Jan. 2000, doi: 10.1016/S0896-6273(00)80886-7.
F. Panza et al., “Apolipoprotein E genotypes and neuropsychiatric symptoms and syndromes in late-onset Alzheimer’s disease,” Ageing Research Reviews, vol. 11, no. 1, pp. 87–103, Jan. 2012, doi: 10.1016/j.arr.2011.06.005.
A. F. Jorm, “History of Depression as a Risk Factor for Dementia: An Updated Review,” Aust N Z J Psychiatry, vol. 35, no. 6, pp. 776–781, Dec. 2001, doi: 10.1046/j.1440-1614.2001.00967.x.
O. P. Almeida, G. J. Hankey, B. B. Yeap, J. Golledge, and L. Flicker, “Depression as a modifiable factor to decrease the risk of dementia,” Transl Psychiatry, vol. 7, no. 5, pp. e1117–e1117, May 2017, doi: 10.1038/tp.2017.90.
V. M. Dotson, M. A. Beydoun, and A. B. Zonderman, “Recurrent depressive symptoms and the incidence of dementia and mild cognitive impairment,” Neurology, vol. 75, no. 1, pp. 27–34, Jul. 2010, doi: 10.1212/WNL.0b013e3181e62124.
R. C. Green et al., “Depression as a Risk Factor for Alzheimer Disease: The MIRAGE Study,” Arch Neurol, vol. 60, no. 5, p. 753, May 2003, doi: 10.1001/archneur.60.5.753.
R. S. Duman, “NEUROBIOLOGY OF STRESS, DEPRESSION, AND RAPID ACTING ANTIDEPRESSANTS: REMODELING SYNAPTIC CONNECTIONS: Review: Remodeling Synaptic Connections,” Depress Anxiety, vol. 31, no. 4, pp. 291–296, Apr. 2014, doi: 10.1002/da.22227.
A. P. Hermida, W. M. McDonald, K. Steenland, and A. Levey, “The association between late-life depression, mild cognitive impairment and dementia: is inflammation the missing link?,” Expert Review of Neurotherapeutics, vol. 12, no. 11, pp. 1339–1350, Nov. 2012, doi: 10.1586/ern.12.127.
K. N. Green, L. M. Billings, B. Roozendaal, J. L. McGaugh, and F. M. LaFerla, “Glucocorticoids Increase Amyloid-β and Tau Pathology in a Mouse Model of Alzheimer’s Disease,” J. Neurosci., vol. 26, no. 35, pp. 9047–9056, Aug. 2006, doi: 10.1523/JNEUROSCI.2797-06.2006.
J. Popp et al., “Cerebrospinal fluid cortisol and clinical disease progression in MCI and dementia of Alzheimer’s type,” Neurobiology of Aging, vol. 36, no. 2, pp. 601–607, Feb. 2015, doi: 10.1016/j.neurobiolaging.2014.10.031.
K. Bisht, K. Sharma, and M.-È. Tremblay, “Chronic stress as a risk factor for Alzheimer’s disease: Roles of microglia-mediated synaptic remodeling, inflammation, and oxidative stress,” Neurobiology of Stress, vol. 9, pp. 9–21, Nov. 2018, doi: 10.1016/j.ynstr.2018.05.003.
K. Ghosal, D. L. Vogt, M. Liang, Y. Shen, B. T. Lamb, and S. W. Pimplikar, “Alzheimer’s disease-like pathological features in transgenic mice expressing the APP intracellular domain,” Proc. Natl. Acad. Sci. U.S.A., vol. 106, no. 43, pp. 18367–18372, Oct. 2009, doi: 10.1073/pnas.0907652106.
N. Origlia et al., “Receptor for Advanced Glycation End Product-Dependent Activation of p38 Mitogen-Activated Protein Kinase Contributes to Amyloid-β-Mediated Cortical Synaptic Dysfunction,” J. Neurosci., vol. 28, no. 13, pp. 3521–3530, Mar. 2008, doi: 10.1523/JNEUROSCI.0204-08.2008.
“Depression in Neurodegenerative Diseases - Common Mechanisms and Current Treatment Options | PDF | Major Depressive Disorder | Hippocampus,” Scribd. Accessed: Apr. 12, 2024. [Online]. Available: https://www.scribd.com/document/520581607/Depression-in-Neurodegenerative-Diseases-Common-Mechanisms-and-Current-Treatment-Options
E. R. Dorsey et al., “Projected number of people with Parkinson disease in the most populous nations, 2005 through 2030,” Neurology, vol. 68, no. 5, pp. 384–386, Jan. 2007, doi: 10.1212/01.wnl.0000247740.47667.03.
L. M. Deuel and L. C. Seeberger, “Complementary Therapies in Parkinson Disease: a Review of Acupuncture, Tai Chi, Qi Gong, Yoga, and Cannabis,” Neurotherapeutics, vol. 17, no. 4, pp. 1434–1455, Oct. 2020, doi: 10.1007/s13311-020-00900-y.
A. Sauerbier, P. Jenner, A. Todorova, and K. R. Chaudhuri, “Non motor subtypes and Parkinson’s disease,” Parkinsonism & Related Disorders, vol. 22, pp. S41–S46, Jan. 2016, doi: 10.1016/j.parkreldis.2015.09.027.
Y. Bang, J. Lim, and H. J. Choi, “Recent advances in the pathology of prodromal non-motor symptoms olfactory deficit and depression in Parkinson’s disease: clues to early diagnosis and effective treatment,” Arch. Pharm. Res., vol. 44, no. 6, pp. 588–604, Jun. 2021, doi: 10.1007/s12272-021-01337-3.
L. Ephraty et al., “Neuropsychiatric and cognitive features in autosomal‐recessive early parkinsonism due to PINK1 mutations,” Movement Disorders, vol. 22, no. 4, pp. 566–569, Mar. 2007, doi: 10.1002/mds.21319.
D. Aarsland, S. Påhlhagen, C. G. Ballard, U. Ehrt, and P. Svenningsson, “Depression in Parkinson disease—epidemiology, mechanisms and management,” Nat Rev Neurol, vol. 8, no. 1, pp. 35–47, Jan. 2012, doi: 10.1038/nrneurol.2011.189.
H. Gustafsson, A. Nordström, and P. Nordström, “Depression and subsequent risk of Parkinson disease: A nationwide cohort study,” Neurology, vol. 84, no. 24, pp. 2422–2429, Jun. 2015, doi: 10.1212/WNL.0000000000001684.
A. F. Leentjens, “Depression—risk factor or early symptom in Parkinson disease?,” Nat Rev Neurol, vol. 11, no. 8, pp. 432–433, Aug. 2015, doi: 10.1038/nrneurol.2015.126.
B. Ravina et al., “The relationship between CAG repeat length and clinical progression in Huntington’s disease,” Movement Disorders, vol. 23, no. 9, pp. 1223–1227, Jul. 2008, doi: 10.1002/mds.21988.
T. Stępień, “Neurogenesis in neurodegenerative diseases in the adult human brain,” Adv Psychiatry Neurol, vol. 30, no. 4, pp. 287–292, 2021, doi: 10.5114/ppn.2021.111950.
S. E. Lazic et al., “Decreased hippocampal cell proliferation in R6/1 Huntington’s mice:,” NeuroReport, vol. 15, no. 5, pp. 811–813, Apr. 2004, doi: 10.1097/00001756-200404090-00014.
M. Czeredys, V. A. Vigont, V. A. Boeva, K. Mikoshiba, E. V. Kaznacheyeva, and J. Kuznicki, “Huntingtin-Associated Protein 1A Regulates Store-Operated Calcium Entry in Medium Spiny Neurons From Transgenic YAC128 Mice, a Model of Huntington’s Disease,” Front. Cell. Neurosci., vol. 12, Oct. 2018, doi: 10.3389/fncel.2018.00381.
K. Duff, J. S. Paulsen, L. J. Beglinger, D. R. Langbehn, and J. C. Stout, “Psychiatric Symptoms in Huntington’s Disease before Diagnosis: The Predict-HD Study,” Biological Psychiatry, vol. 62, no. 12, pp. 1341–1346, Dec. 2007, doi: 10.1016/j.biopsych.2006.11.034.
A. K. Ho, A. S. Gilbert, S. L. Mason, A. O. Goodman, and R. A. Barker, “Health‐related quality of life in Huntington’s disease: Which factors matter most?,” Movement Disorders, vol. 24, no. 4, pp. 574–578, Mar. 2009, doi: 10.1002/mds.22412.
P. McColgan et al., “Structural and functional brain network correlates of depressive symptoms in premanifest Huntington’s disease,” Human Brain Mapping, vol. 38, no. 6, pp. 2819–2829, Jun. 2017, doi: 10.1002/hbm.23527.
G. R. Poudel et al., “Functional Brain Correlates of Neuropsychiatric Symptoms in Presymptomatic Huntington’s Disease: The IMAGE-HD Study,” JHD, vol. 4, no. 4, pp. 325–332, Dec. 2015, doi: 10.3233/JHD-150154.
M. E. Castro, J. Pascual, T. Romón, J. Berciano, J. Figols, and A. Pazos, “5-HT1B receptor binding in degenerative movement disorders,” Brain Research, vol. 790, no. 1–2, pp. 323–328, Apr. 1998, doi: 10.1016/S0006-8993(97)01566-7.
G. Livingston et al., “Dementia prevention, intervention, and care,” The Lancet, vol. 390, no. 10113, pp. 2673–2734, Dec. 2017, doi: 10.1016/S0140-6736(17)31363-6.
A. Tolppanen et al., “Leisure‐time physical activity from mid‐ to late life, body mass index, and risk of dementia,” Alzheimer’s & Dementia, vol. 11, no. 4, p. 434, Apr. 2015, doi: 10.1016/j.jalz.2014.01.008.
EPD Study Group et al., “Physical exercise for prevention of dementia (EPD) study: background, design and methods,” BMC Public Health, vol. 19, no. 1, p. 659, Dec. 2019, doi: 10.1186/s12889-019-7027-3.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2024 Sara Rosołowska-Żak, Maria Sambura, Wiktoria Sas, Katarzyna Podyma, Gracja Ryznar, Julia Rejdych, Piotr Pierzchała, Michalina Minkowska, Krystyna Chimiak, Gabriela Bylica
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
Stats
Number of views and downloads: 260
Number of citations: 0
