Association between widespread pain and dementia, Alzheimer’s disease and stroke: a cohort study from the Framingham Heart Study

2021 ◽  
pp. rapm-2021-102733
Author(s):  
Kanran Wang ◽  
Hong Liu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Chronic Pain ◽  
Cohort Study ◽  
Framingham Heart Study ◽  
Widespread Pain ◽  
Dementia Risk ◽  
Heart Study ◽  
Alzheimer’S Disease Dementia

Background and objectiveChronic pain may be an early indicator of cognitive decline, but previous studies have not systematically examined the population-level associations between widespread pain and adverse cognitive outcomes and stroke. This study was designed to determine the association between widespread pain, a common subtype of chronic pain, and subsequent dementia, Alzheimer’s disease dementia and stroke.MethodsThis retrospective cohort study used data from the US community-based Framingham Heart Study. Pain status was assessed at a single time point between 1990 and 1994. Widespread pain was determined based on the Framingham Heart Study pain homunculus. Dementia follow-up occurred across a median of 10 years (IQR, 6–13 years) for persons who were dementia free at baseline. Proportional hazard models examined associations between widespread pain and incident dementia, Alzheimer’s disease dementia and stroke.ResultsA total of 347 (14.1%) subjects fulfilled the criteria for widespread pain, whereas 2117 (85.9%) subjects did not. Of 188 cases of incident all-cause dementia, 128 were Alzheimer’s disease dementia. In addition, 139 patients suffered stroke during the follow-up period. After multivariate adjustment including age and sex, widespread pain was associated with 43% increase in all-cause dementia risk (HR: 1.43; 95% CI 1.06 to 1.92), 47% increase in Alzheimer’s disease dementia risk (HR: 1.47; 95% CI 1.13 to 2.20) and 29% increase in stroke risk (HR: 1.29; 95% CI 1.08 to 2.54). Comparable results were shown in the subgroup of individuals over 65 years old.ConclusionWidespread pain was associated with an increased incidence of all-cause dementia, Alzheimer’s disease dementia and stroke.Trial registration numberNCT00005121.

Associations of loneliness with risk of Alzheimer's disease dementia in the Framingham Heart Study

2021 ◽  
Author(s):  
Samia C. Akhter‐Khan ◽  
Qiushan Tao ◽  
Ting Fang Alvin Ang ◽  
Indira Swetha Itchapurapu ◽  
Michael L. Alosco ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Framingham Heart Study ◽  
Heart Study ◽  
Alzheimer’S Disease Dementia

scholarly journals Non-Cancer Chronic Pain Conditions and Risk for Incident Alzheimer’s Disease and Related Dementias in Community-Dwelling Older Adults: A Population-Based Retrospective Cohort Study of United States Medicare Beneficiaries, 2001–2013

2020 ◽  
Vol 17 (15) ◽  
pp. 5454
Author(s):  
Sumaira Khalid ◽  
Usha Sambamoorthi ◽  
Kim E. Innes
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Chronic Pain ◽  
Cohort Study ◽  
Sleep Disorders ◽  
Retrospective Cohort Study ◽  
Retrospective Cohort ◽  
Community Dwelling ◽  
Chronic Pain Conditions

Accumulating evidence suggests that certain chronic pain conditions may increase risk for incident Alzheimer’s disease and related dementias (ADRD). Rigorous longitudinal research remains relatively sparse, and the relation of overall chronic pain condition burden to ADRD risk remains little studied, as has the potential mediating role of sleep and mood disorders. In this retrospective cohort study, we investigated the association of common non-cancer chronic pain conditions (NCPC) at baseline to subsequent risk for incident ADRD, and assessed the potential mediating effects of mood and sleep disorders, using baseline and 2-year follow-up data using 11 pooled cohorts (2001–2013) drawn from the U.S. Medicare Current Beneficiaries Survey (MCBS). The study sample comprised 16,934 community-dwelling adults aged ≥65 and ADRD-free at baseline. NCPC included: headache, osteoarthritis, joint pain, back or neck pain, and neuropathic pain, ascertained using claims data; incident ADRD (N = 1149) was identified using claims and survey data. NCPC at baseline remained associated with incident ADRD after adjustment for sociodemographics, lifestyle characteristics, medical history, medications, and other factors (adjusted odds ratio (AOR) for any vs. no NCPC = 1.21, 95% confidence interval (CI) = 1.04–1.40; p = 0.003); the strength and magnitude of this association rose significantly with increasing number of diagnosed NCPCs (AOR for 4+ vs. 0 conditions = 1.91, CI = 1.31–2.80, p-trend < 0.00001). Inclusion of sleep disorders and/or depression/anxiety modestly reduced these risk estimates. Sensitivity analyses yielded similar findings. NCPC was significantly and positively associated with incident ADRD; this association may be partially mediated by mood and sleep disorders. Additional prospective studies with longer-term follow-up are warranted to confirm and extend our findings.

scholarly journals Genetic Interaction with Plasma Lipids on Alzheimer’s Disease in the Framingham Heart Study

2018 ◽  
Vol 66 (3) ◽  
pp. 1275-1282
Author(s):  
Gina M. Peloso ◽  
Alexa S. Beiser ◽  
Anita L. Destefano ◽  
Sudha Seshadri
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Framingham Heart Study ◽  
Plasma Lipids ◽  
Genetic Interaction ◽  
Heart Study

Childhood Secondhand Smoke Exposure and Risk of Dementia, Alzheimer’s Disease and Stroke in Adulthood: A Prospective Cohort Study

2021 ◽  
pp. 1-6
Author(s):  
S. Zhou ◽  
K. Wang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Secondhand Smoke ◽  
Smoking Status ◽  
Smoke Exposure ◽  
Secondhand Smoke Exposure ◽  
Heart Study ◽  
Wide Range ◽  
Exposure To Secondhand Smoke

Background: This study aimed to investigate the associations between secondhand smoke exposure and dementia, Alzheimer’s disease (AD) and stroke. Methods: This prospective study analyzed Framingham Offspring (FHS-OS) cohort participants with parents in the original Framingham Heart Study (FHS) cohort with known smoking status during offspring childhood. Surveillance for incident events, including dementia and stroke, among offspring participants exposed to parental smoking up to the age of 18 years commenced at examination 9 through 2014 and continued for approximately 30 years. Results: At baseline, a total of 1683 (56.2%) subjects were not exposed to any secondhand smoke, whereas 670 (22.4%) subjects were exposed to 0-1 packs (20 cigarettes)/day, and 640 (21.4%) were exposed to over 1 pack/day. On follow-up (median: 31 years), 2993 patients developed dementia, including 103 with AD dementia and 315 with stroke. After adjusting for a wide range of established risk factors, participants with the highest exposure to secondhand smoke exhibited increased risks of all dementia, AD dementia and stroke compared with individuals with no exposure [HR 2.86 (2.00-4.09) for dementia; HR 3.13 (1.80-5.42) for AD dementia; HR 1.89 (1.37-2.61) for stroke]. The results remained comparable in the subgroup for individuals with median exposure to secondhand smoke. Conclusion: Exposure to secondhand smoke may be associated with increased risks of dementia, AD dementia and stroke.

Ozone, Particulate Matter, and Newly Diagnosed Alzheimer’s Disease: A Population-Based Cohort Study in Taiwan

2021 ◽  
Author(s):  
Chau-Ren Jung ◽  
Yu-Ting Lin ◽  
Bing-Fang Hwang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Air Pollution ◽  
Cohort Study ◽  
Particulate Matter ◽  
Proportional Hazards ◽  
Newly Diagnosed ◽  
Hazards Model

Several studies with animal research associate air pollution in Alzheimer’s disease (AD) neuropathology, but the actual impact of air pollution on the risk of AD is unknown. Here, this study investigates the association between long-term exposure to ozone (O3) and particulate matter (PM) with an aerodynamic diameter equal to or less than 2.5 μm (PM2.5), and newly diagnosed AD in Taiwan. We conducted a cohort study of 95,690 individuals’ age ≥ 65 during 2001–2010. We obtained PM10 and O3 data from Taiwan Environmental Protection Agency during 2000–2010. Since PM2.5 data is only accessible entirely after 2006, we used the mean ratio between PM2.5 and PM10 during 2006–2010 (0.57) to estimate the PM2.5 concentrations from 2000 to 2005. A Cox proportional hazards model was used to evaluate the associations between O3 and PM2.5 at baseline and changes of O3 and PM2.5 during the follow-up period and AD. The adjusted HR for AD was weakly associated with a raised concentration in O3 at baseline per increase of 9.63 ppb (adjusted HR 1.06, 95% confidence interval (CI) 1.00–1.12). Further, we estimated a 211% risk of increase of AD per increase of 10.91 ppb in O3 over the follow-up period (95% CI 2.92–3.33). We found a 138% risk of increase of AD per increase of 4.34 μg/m3 in PM2.5 over the follow-up period (95% CI 2.21–2.56). These findings suggest long-term exposure to O3 and PM2.5 above the current US EPA standards are associated with increased the risk of AD.

scholarly journals 0419 IL-6 Moderates the Association Between Obstructive Sleep Apnea Severity and Incident Alzheimer’s Disease: The Framingham Heart Study

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A160-A161
Author(s):  
A Baril ◽  
A S Beiser ◽  
S Redline ◽  
E R McGrath ◽  
H J Aparicio ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Sleep Duration ◽  
Framingham Heart Study ◽  
Sleep Disturbances ◽  
Heart Study ◽  
Obstructive Sleep

Abstract Introduction Both sleep disturbances and inflammation are potential risk factors for Alzheimer’s disease (AD). However, it is unknown how inflammation and sleep interact together to influence the risk of developing AD dementia. Our objective was to evaluate whether interleukin-6 (IL-6) levels interact with sleep disturbances when predicting incident clinical AD. Methods We studied participants in the Framingham Heart Study Offspring cohort who completed in-home overnight polysomnography. Sleep characteristics were continuous and included sleep duration, wake after sleep onset (WASO), and apnea-hypopnea index (AHI). Participants were stratified into quartiles of IL-6 levels. Surveillance for incident AD dementia occurred over a mean follow-up of 13.4±5.4 years. Using Cox proportional hazards regression models, we tested the interaction of sleep measures by IL-6 quartiles on incident AD dementia. All analyses adjusted for age and sex and P&lt;0.05 was considered significant. Results The final sample included 291 dementia-free participants at baseline (age 67.5±4.9 years, 51.6% men). Approximately one quarter of participants had obstructive sleep apnea (OSA; AHI&gt;15) at baseline (median:6.2, Q1:2,3, Q3:14.3). We observed 33 cases of incident AD dementia during follow-up. Although no interaction was observed for either sleep duration or WASO with IL-6 levels, there was a significant interaction of AHI with IL-6 in predicting AD dementia (p=0.002). In the lowest IL-6 quartile, higher AHI was associated with an elevated risk of AD dementia (hazard ratio, 4.15 [95%CI, 1.42, 12.1], p=0.01) whereas no association between AHI and incident AD was observed in other IL-6 quartiles. Conclusion Our findings suggest that the pro-inflammatory cytokine IL-6 moderates the association between OSA and incident AD risk. The association between increasing OSA severity and incident AD was only observed in those with lower IL-6 levels, suggesting that this association might be especially apparent when no other confounding risk factors such as inflammation are present. Support The Framingham Heart Study is supported by contracts from the National Heart, Lung and Blood Institute, grants from the National Institute on Aging, and grants from the National Institute of Neurological Disorders and Stroke.

scholarly journals Plasma tau, neurofilament light chain and amyloid-β levels and risk of dementia; a population-based cohort study

Brain ◽  
2020 ◽  
Vol 143 (4) ◽  
pp. 1220-1232 ◽  
Author(s):  
Frank de Wolf ◽  
Mohsen Ghanbari ◽  
Silvan Licher ◽  
Kevin McRae-McKee ◽  
Luuk Gras ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Plasma Levels ◽  
Amyloid Β ◽  
Neurofilament Light Chain ◽  
Neurofilament Light ◽  
Total Tau ◽  
Quartile Group ◽  
Alzheimer’S Disease Dementia

Abstract CSF biomarkers, including total-tau, neurofilament light chain (NfL) and amyloid-β, are increasingly being used to define and stage Alzheimer’s disease. These biomarkers can be measured more quickly and less invasively in plasma and may provide important information for early diagnosis of Alzheimer’s disease. We used stored plasma samples and clinical data obtained from 4444 non-demented participants in the Rotterdam study at baseline (between 2002 and 2005) and during follow-up until January 2016. Plasma concentrations of total-tau, NfL, amyloid-β40 and amyloid-β42 were measured using the Simoa NF-light® and N3PA assays. Associations between biomarker plasma levels and incident all-cause and Alzheimer’s disease dementia during follow-up were assessed using Cox proportional-hazard regression models adjusted for age, sex, education, cardiovascular risk factors and APOE ε4 status. Moreover, biomarker plasma levels and rates of change over time of participants who developed Alzheimer’s disease dementia during follow-up were compared with age and sex-matched dementia-free control subjects. During up to 14 years follow-up, 549 participants developed dementia, including 374 cases with Alzheimer’s disease dementia. A log2 higher baseline amyloid-β42 plasma level was associated with a lower risk of developing all-cause or Alzheimer’s disease dementia, adjusted hazard ratio (HR) 0.61 [95% confidence interval (CI), 0.47–0.78; P &lt; 0.0001] and 0.59 (95% CI, 0.43–0.79; P = 0.0006), respectively. Conversely, a log2 higher baseline plasma NfL level was associated with a higher risk of all-cause dementia [adjusted HR 1.59 (95% CI, 1.38–1.83); P &lt; 0.0001] or Alzheimer’s disease [adjusted HR 1.50 (95% CI, 1.26–1.78); P &lt; 0.0001]. Combining the lowest quartile group of amyloid-β42 with the highest of NfL resulted in a stronger association with all-cause dementia [adjusted HR 9.5 (95% CI, 2.3–40.4); P &lt; 0.002] and with Alzheimer’s disease [adjusted HR 15.7 (95% CI, 2.1–117.4); P &lt; 0.0001], compared to the highest quartile group of amyloid-β42 and lowest of NfL. Total-tau and amyloid-β40 levels were not associated with all-cause or Alzheimer’s disease dementia risk. Trajectory analyses of biomarkers revealed that mean NfL plasma levels increased 3.4 times faster in participants who developed Alzheimer’s disease compared to those who remained dementia-free (P &lt; 0.0001), plasma values for cases diverged from controls 9.6 years before Alzheimer’s disease diagnosis. Amyloid-β42 levels began to decrease in Alzheimer’s disease cases a few years before diagnosis, although the decline did not reach significance compared to dementia-free participants. In conclusion, our study shows that low amyloid-β42 and high NfL plasma levels are each independently and in combination strongly associated with risk of all-cause and Alzheimer’s disease dementia. These data indicate that plasma NfL and amyloid-β42 levels can be used to assess the risk of developing dementia in a non-demented population. Plasma NfL levels, although not specific, may also be useful in monitoring progression of Alzheimer’s disease dementia.

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