Osteoarthritis Was Associated With a Faster Decline in Hippocampal Volumes in Cognitively Normal Older People

Xiang Li, Qiaowen Tong, Jianqing Gao, Cailong Liu, Alzheimer’s Disease Neuroimaging Initiative, Yangbo Liu, Xiang Li, Qiaowen Tong, Jianqing Gao, Cailong Liu, Alzheimer’s Disease Neuroimaging Initiative, Yangbo Liu

Abstract

Objective: To examine whether osteoarthritis (OA) is associated with a change in adjusted hippocampal volumes (HpVR: hippocampal/intracranial volume × 103) over time among cognitively normal older people.

Methods: We examined the cross-sectional and longitudinal associations of OA with HpVR among individuals with normal cognition (NC) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study. At baseline, a total of 372 individuals with NC were included.

Results: In the cross-sectional analyses of baseline data, we did not find a significant relationship between OA and HpVR among individuals with NC. However, in the longitudinal analyses, OA was significantly associated with change in HpVR over time among individuals with NC. Specifically, compared with individuals without OA, those with OA showed a faster decline in HpVR over time when controlling for other potential confounders, including age, educational attainment, gender, and APOE4 genotype.

Conclusion: OA status was significantly associated with a change in HpVR over time among individuals with NC.

Keywords: Alzheimer’s disease; hippocampal volumes; longitudinal study; normal cognition; osteoarthritis.

Copyright © 2020 Li, Tong, Gao, Liu and Liu.

Figures

FIGURE 1
FIGURE 1
Flowchart of the data selections at baseline.
FIGURE 2
FIGURE 2
Cross-sectional association of OA with MMSE, ADAS-Cog11, and HpVR among individuals with NC. There was no significant difference in MMSE, ADAS-Cog11, or HpVR between the two groups (all p > 0.05). OA: osteoarthritis; MMSE: mini-mental state examination; ADAS-Cog 11: Alzheimer’s disease assessment scale-cognitive 11-item. HpVR: hippocampal volume ratio (HpVR, hippocampal/intracranial volume × 103).
FIGURE 3
FIGURE 3
Association of OA status with conversion from NC to MCI or AD dementia. OA status was not associated with conversion from NC to MCI or AD dementia (OA + : HR = 1.6, se = 0.28, p = 0.09). OA: osteoarthritis; NC: normal cognition; MCI: mild cognitive impairment; AD: Alzheimer’s disease.
FIGURE 4
FIGURE 4
Association of OA with change in HpVR among individuals with NC. Compared with individuals without OA, those with OA showed a significantly steeper decline in HpVR (estimate: –0.0161, p = 0.0059) after adjusting for other potential confounders. OA: osteoarthritis; HpVR: hippocampal volume ratio (HpVR, hippocampal/intracranial volume × 103).

References

    1. Block M. L., Zecca L., Hong J. S. (2007). Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. Nat. Rev. Neurosci. 8 57–69. 10.1038/nrn2038
    1. Buchman A. S., Boyle P. A., Yu L., Shah R. C., Wilson R. S., Bennett D. A. (2012). Total daily physical activity and the risk of AD and cognitive decline in older adults. Neurology 78 1323–1329. 10.1212/wnl.0b013e3182535d35
    1. Chen K. T., Chen Y. C., Fan Y. H., Lin W. X., Lin W. C., Wang Y. H., et al. (2018). Rheumatic diseases are associated with a higher risk of dementia: a nation-wide, population-based, case-control study. Int. J. Rheum. Dis. 21 373–380. 10.1111/1756-185x.13246
    1. Folstein M. F., Folstein S. E., Mchugh P. R. (1975). Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J. Psychiatr. Res. 12 189–198.
    1. Goldring M. B., Suen L. F., Yamin R., Lai W. F. (1996). Regulation of Collagen Gene Expression by Prostaglandins and Interleukin-1beta in Cultured Chondrocytes and Fibroblasts. Am. J. Ther. 3 9–16. 10.1097/00045391-199601000-00003
    1. Heneka M. T., Carson M. J., El Khoury J., Landreth G. E., Brosseron F., Feinstein D. L., et al. (2015). Neuroinflammation in Alzheimer’s disease. Lancet Neurol. 14 388–405.
    1. Holmes C., Cunningham C., Zotova E., Woolford J., Dean C., Kerr S., et al. (2009). Systemic inflammation and disease progression in Alzheimer disease. Neurology 73 768–774. 10.1212/wnl.0b013e3181b6bb95
    1. Huang S.-W., Wang W.-T., Chou L.-C., Liao C.-D., Liou T.-H., Lin H.-W. (2015). Osteoarthritis increases the risk of dementia: a nationwide cohort study in Taiwan. Sci. Rep. 5:10145.
    1. Hunter D. J., Bierma-Zeinstra S. (2019). Osteoarthritis. Lancet 393 1745–1759.
    1. Jack C. R., Jr., Bernstein M. A., Fox N. C., Thompson P., Alexander G., Harvey D., et al. (2008). The Alzheimer’s Disease Neuroimaging Initiative (ADNI): MRI methods. J. Magn. Reson. Imaging 27 685–691.
    1. Kyrkanides S., Tallents R. H., Jen-Nie H. M., Olschowka M. E., Johnson R., Yang M., et al. (2011). Osteoarthritis accelerates and exacerbates Alzheimer’s disease pathology in mice. J. Neuroinflam. 8:112. 10.1186/1742-2094-8-112
    1. Liu Y., Tan L., Wang H. F., Liu Y., Hao X. K., Tan C. C., et al. (2016). Multiple Effect of APOE genotype on clinical and neuroimaging biomarkers across Alzheimer’s disease spectrum. Mol. Neurobiol. 53 4539–4547. 10.1007/s12035-015-9388-7
    1. Martel-Pelletier J., Alaaeddine N., Pelletier J. P. (1999). Cytokines and their role in the pathophysiology of osteoarthritis. Front. Biosci. 4:D694–D703. 10.2741/martel
    1. Morales I., Guzman-Martinez L., Cerda-Troncoso C., Farias G. A., Maccioni R. B. (2014). Neuroinflammation in the pathogenesis of Alzheimer’s disease. A rational framework for the search of novel therapeutic approaches. Front. Cell Neurosci. 8:112. 10.3389/fncel.2014.00112
    1. Morris J. C. (1993). The Clinical Dementia Rating (CDR): current version and scoring rules. Neurology 43 2412–2414.
    1. Querfurth H. W., Laferla F. M. (2010). Alzheimer’s disease. N. Engl. J. Med. 362 329–344.
    1. Tan Z., Beiser A., Vasan R., Roubenoff R., Dinarello C., Harris T., et al. (2007). Inflammatory markers and the risk of Alzheimer disease: the Framingham Study. Neurology 68 1902–1908. 10.1212/01.wnl.0000263217.36439.da
    1. Tan Z. S., Spartano N. L., Beiser A. S., Decarli C., Auerbach S. H., Vasan R. S., et al. (2017). Physical activity, brain volume, and dementia risk: the framingham study. J. Gerontol. A Biol. Sci. Med. Sci. 72 789–795.
    1. Wang J. H., Wu Y. J., Tee B. L., Lo R. Y. (2018). Medical comorbidity in Alzheimer’s disease: a nested case-control study. J. Alzheimers. Dis. 63 773–781. 10.3233/jad-170786
    1. Weber A., Hung Mak S., Berenbaum F., Sellam J., Zheng Y.-P., Han Y., et al. (2019). Association between osteoarthritis and increased risk of dementia: a systemic review and meta-analysis. Medicine 98:e14355. 10.1097/md.0000000000014355
    1. Westacott C. I., Sharif M. (1996). Cytokines in osteoarthritis: mediators or markers of joint destruction? Semin. Arthritis Rheum. 25 254–272. 10.1016/s0049-0172(96)80036-9
    1. Zhang F., Jiang L. (2015). Neuroinflammation in Alzheimer’s disease. Neuropsychiatr. Dis. Treat. 11 243–256.

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