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High Blood caffeine levels in MCI linked to lack of progression to dementia.

ABSTRACT: Although both human epidemiologic and animal model studies have suggested that caffeine/coffee protects against Alzheimer's disease, direct human evidence for this premise has been lacking. In the present case-control study, two separate cohorts consisting of 124 total individuals (65-88 years old) were cognitively assessed and a blood sample taken for caffeine/biomarker analysis. Subjects were then monitored for cognitive status over the ensuing 2-4 year period to determine the extent to which initial plasma caffeine/biomarkers levels would be predictive of changes in cognitive status. Plasma caffeine levels at study onset were substantially lower (-51%) in mild cognitive impairment (MCI) subjects who later progressed to dementia (MCI?DEM) compared to levels in stable MCI subjects (MCI?MCI). Moreover, none of the MCI?DEM subjects had initial blood caffeine levels that were above a critical level of 1200 ng/ml, while half of stable MCI?MCI subjects had blood caffeine levels higher than that critical level. Thus, plasma caffeine levels greater than 1200 ng/ml (?6 ?M) in MCI subjects were associated with no conversion to dementia during the ensuing 2-4 year follow-up period. Among the 11 cytokines measured in plasma, three of them (GCSF, IL-10, and IL-6) were decreased in MCI?DEM subjects, but not in stable MCI?MCI subjects with high plasma caffeine levels. Coffee would appear to be the major or perhaps only source of caffeine for such stable MCI patients. This case-control study provides the first direct evidence that caffeine/coffee intake is associated with a reduced risk of dementia or delayed onset, particularly for those who already have MCI.

SUBMITTER: Cao C

PROVIDER: S-EPMC5592113 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

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High Blood caffeine levels in MCI linked to lack of progression to dementia.

Cao Chuanhai C Loewenstein David A DA Lin Xiaoyang X Zhang Chi C Wang Li L Duara Ranjan R Wu Yougui Y Giannini Alessandra A Bai Ge G Cai Jianfeng J Greig Maria M Schofield Elizabeth E Ashok Raj R Small Brent B Potter Huntington H Arendash Gary W GW

Journal of Alzheimer's disease : JAD 20120101 3

Although both human epidemiologic and animal model studies have suggested that caffeine/coffee protects against Alzheimer's disease, direct human evidence for this premise has been lacking. In the present case-control study, two separate cohorts consisting of 124 total individuals (65-88 years old) were cognitively assessed and a blood sample taken for caffeine/biomarker analysis. Subjects were then monitored for cognitive status over the ensuing 2-4 year period to determine the extent to which ...[more]

PMID: 22430531

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Project description:ObjectiveThe objective of this study was to examine the association between caffeine intake and cognitive impairment. Caffeine-neuropathology correlations and interactions with lifestyle and genetic factors impacting caffeine metabolism and response were also tested.MethodsWe included 888 participants aged 59+ years from the Rush Memory and Aging Project (MAP) and 303,887 participants aged 55+ years from the UK Biobank (UKB). MAP participants took part in annual cognitive testing. Diagnosis of dementia was based on clinical neurological examination and standardized criteria. A subset provided postmortem tissue for neuropathologic evaluation for common age-related diseases (eg, Alzheimer's disease [AD], Lewy bodies, and vascular). For UKB, dementia was determined by linked hospital and death records. Self-reported caffeine intake was estimated using food-frequency questionnaires in both cohorts. Cox proportional hazard ratio (HR), regression, and mixed models were used to examine associations of caffeine intake with incident dementia, cognitive decline, and neuropathology.ResultsIn MAP, compared to ≤100 mg/day, caffeine intake >100 mg/day was associated with a significantly higher HR (95% confidence interval [CI]) of all-cause (HR = 1.35, 95% CI = 1.03-1.76) and AD (HR = 1.41, 95% CI = 1.07-1.85) dementia. Caffeine intake was not associated with cognitive decline. In UKB, compared to ≤100 mg/day, the HRs (95% CI) of all-cause dementia for consuming 100 ≤ 200, 200 ≤ 300, 300 ≤ 400, and > 400 mg/day were 0.83 (95% CI = 0.72-0.94), 0.74 (95% CI = 0.64-0.85), 0.74 (95% CI = 0.64-0.85), and 0.92 (95% CI = 0.79-1.08), respectively. Similar results were observed for Alzheimer's dementia. In MAP, caffeine intake was inversely associated with postmortem Lewy bodies but no other age-related pathologies. Caffeine intake >100 mg/day was associated with lower neocortical type Lewy bodies (odds ratio (95%CI): 0.40 (95% CI = 0.21-0.75).InterpretationCaffeine intake was inconsistently associated with clinical dementia; potentially explained by cohort differences in underlying dementia etiology. Lewy bodies may link caffeine to lower risk in some persons. ANN NEUROL 2022;91:834-846.

Dataset Information

High Blood caffeine levels in MCI linked to lack of progression to dementia.

Publications

High Blood caffeine levels in MCI linked to lack of progression to dementia.

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