Statins, risk of dementia, and cognitive function: Secondary analysis of the ginkgo evaluation of memory study

Kerstin Bettermann, Alice M. Arnold, Jeff Williamson, Stephen Rapp, Kaycee Sink, James F. Toole, Michelle C. Carlson, Sevil Yasar, Steven Dekosky, Gregory L. Burke

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

Background: Lipid-lowering medications (LLMs) and especially statin drugs can delay cognitive decline and dementia onset in individuals with and without mild cognitive impairment (MCI) at baseline. Methods: A longitudinal, observational study was conducted of 3069 cognitively healthy elderly patients (≥75 years of age) who were enrolled in the Ginkgo Evaluation of Memory Study. The primary outcome measure was the time to adjudicated all-cause dementia and Alzheimer dementia (AD). The secondary outcome measure was the change in global cognitive function over time measured by scores from the Modified Mini-Mental State Exam (3MSE) and the cognitive subscale of the AD Assessment Scale (ADAS-Cog). Results: Among participants without MCI at baseline, the current use of statins was consistently associated with a reduced risk of all-cause dementia (hazard ratio [HR], 0.79; 95% confidence interval [95% CI], 0.65-0.96; P =.021) and AD (HR, 0.57; 95% CI, 0.39-0.85; P =.005). In participants who initiated statin therapy, lipophilic statins tended to reduce dementia risk more than nonlipophilic agents. In contrast, there was no significant association between LLM use (including statins), dementia onset, or cognitive decline in individuals with baseline MCI. However, in individuals without MCI at baseline, there was a trend for a neuroprotective effect of statins on cognitive decline. Conclusions: Statins may slow the rate of cognitive decline and delay the onset of AD and all-cause dementia in cognitively healthy elderly individuals, whereas individuals with MCI may not have comparable cognitive protection from these agents. However, the results from this observational study need to be interpreted with caution and will require confirmation by randomized clinical trials stratifying treatment groups based on MCI status at baseline.

Original languageEnglish (US)
Pages (from-to)436-444
Number of pages9
JournalJournal of Stroke and Cerebrovascular Diseases
Volume21
Issue number6
DOIs
StatePublished - Aug 1 2012

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Hydroxymethylglutaryl-CoA Reductase Inhibitors
Ginkgo biloba
Cognition
Dementia
Alzheimer Disease
Observational Studies
Outcome Assessment (Health Care)
Cognitive Dysfunction
Confidence Intervals
Lipids
Neuroprotective Agents
Longitudinal Studies
Randomized Controlled Trials

All Science Journal Classification (ASJC) codes

  • Surgery
  • Rehabilitation
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

Cite this

Bettermann, Kerstin ; Arnold, Alice M. ; Williamson, Jeff ; Rapp, Stephen ; Sink, Kaycee ; Toole, James F. ; Carlson, Michelle C. ; Yasar, Sevil ; Dekosky, Steven ; Burke, Gregory L. / Statins, risk of dementia, and cognitive function : Secondary analysis of the ginkgo evaluation of memory study. In: Journal of Stroke and Cerebrovascular Diseases. 2012 ; Vol. 21, No. 6. pp. 436-444.
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abstract = "Background: Lipid-lowering medications (LLMs) and especially statin drugs can delay cognitive decline and dementia onset in individuals with and without mild cognitive impairment (MCI) at baseline. Methods: A longitudinal, observational study was conducted of 3069 cognitively healthy elderly patients (≥75 years of age) who were enrolled in the Ginkgo Evaluation of Memory Study. The primary outcome measure was the time to adjudicated all-cause dementia and Alzheimer dementia (AD). The secondary outcome measure was the change in global cognitive function over time measured by scores from the Modified Mini-Mental State Exam (3MSE) and the cognitive subscale of the AD Assessment Scale (ADAS-Cog). Results: Among participants without MCI at baseline, the current use of statins was consistently associated with a reduced risk of all-cause dementia (hazard ratio [HR], 0.79; 95{\%} confidence interval [95{\%} CI], 0.65-0.96; P =.021) and AD (HR, 0.57; 95{\%} CI, 0.39-0.85; P =.005). In participants who initiated statin therapy, lipophilic statins tended to reduce dementia risk more than nonlipophilic agents. In contrast, there was no significant association between LLM use (including statins), dementia onset, or cognitive decline in individuals with baseline MCI. However, in individuals without MCI at baseline, there was a trend for a neuroprotective effect of statins on cognitive decline. Conclusions: Statins may slow the rate of cognitive decline and delay the onset of AD and all-cause dementia in cognitively healthy elderly individuals, whereas individuals with MCI may not have comparable cognitive protection from these agents. However, the results from this observational study need to be interpreted with caution and will require confirmation by randomized clinical trials stratifying treatment groups based on MCI status at baseline.",
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Statins, risk of dementia, and cognitive function : Secondary analysis of the ginkgo evaluation of memory study. / Bettermann, Kerstin; Arnold, Alice M.; Williamson, Jeff; Rapp, Stephen; Sink, Kaycee; Toole, James F.; Carlson, Michelle C.; Yasar, Sevil; Dekosky, Steven; Burke, Gregory L.

In: Journal of Stroke and Cerebrovascular Diseases, Vol. 21, No. 6, 01.08.2012, p. 436-444.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Statins, risk of dementia, and cognitive function

T2 - Secondary analysis of the ginkgo evaluation of memory study

AU - Bettermann, Kerstin

AU - Arnold, Alice M.

AU - Williamson, Jeff

AU - Rapp, Stephen

AU - Sink, Kaycee

AU - Toole, James F.

AU - Carlson, Michelle C.

AU - Yasar, Sevil

AU - Dekosky, Steven

AU - Burke, Gregory L.

PY - 2012/8/1

Y1 - 2012/8/1

N2 - Background: Lipid-lowering medications (LLMs) and especially statin drugs can delay cognitive decline and dementia onset in individuals with and without mild cognitive impairment (MCI) at baseline. Methods: A longitudinal, observational study was conducted of 3069 cognitively healthy elderly patients (≥75 years of age) who were enrolled in the Ginkgo Evaluation of Memory Study. The primary outcome measure was the time to adjudicated all-cause dementia and Alzheimer dementia (AD). The secondary outcome measure was the change in global cognitive function over time measured by scores from the Modified Mini-Mental State Exam (3MSE) and the cognitive subscale of the AD Assessment Scale (ADAS-Cog). Results: Among participants without MCI at baseline, the current use of statins was consistently associated with a reduced risk of all-cause dementia (hazard ratio [HR], 0.79; 95% confidence interval [95% CI], 0.65-0.96; P =.021) and AD (HR, 0.57; 95% CI, 0.39-0.85; P =.005). In participants who initiated statin therapy, lipophilic statins tended to reduce dementia risk more than nonlipophilic agents. In contrast, there was no significant association between LLM use (including statins), dementia onset, or cognitive decline in individuals with baseline MCI. However, in individuals without MCI at baseline, there was a trend for a neuroprotective effect of statins on cognitive decline. Conclusions: Statins may slow the rate of cognitive decline and delay the onset of AD and all-cause dementia in cognitively healthy elderly individuals, whereas individuals with MCI may not have comparable cognitive protection from these agents. However, the results from this observational study need to be interpreted with caution and will require confirmation by randomized clinical trials stratifying treatment groups based on MCI status at baseline.

AB - Background: Lipid-lowering medications (LLMs) and especially statin drugs can delay cognitive decline and dementia onset in individuals with and without mild cognitive impairment (MCI) at baseline. Methods: A longitudinal, observational study was conducted of 3069 cognitively healthy elderly patients (≥75 years of age) who were enrolled in the Ginkgo Evaluation of Memory Study. The primary outcome measure was the time to adjudicated all-cause dementia and Alzheimer dementia (AD). The secondary outcome measure was the change in global cognitive function over time measured by scores from the Modified Mini-Mental State Exam (3MSE) and the cognitive subscale of the AD Assessment Scale (ADAS-Cog). Results: Among participants without MCI at baseline, the current use of statins was consistently associated with a reduced risk of all-cause dementia (hazard ratio [HR], 0.79; 95% confidence interval [95% CI], 0.65-0.96; P =.021) and AD (HR, 0.57; 95% CI, 0.39-0.85; P =.005). In participants who initiated statin therapy, lipophilic statins tended to reduce dementia risk more than nonlipophilic agents. In contrast, there was no significant association between LLM use (including statins), dementia onset, or cognitive decline in individuals with baseline MCI. However, in individuals without MCI at baseline, there was a trend for a neuroprotective effect of statins on cognitive decline. Conclusions: Statins may slow the rate of cognitive decline and delay the onset of AD and all-cause dementia in cognitively healthy elderly individuals, whereas individuals with MCI may not have comparable cognitive protection from these agents. However, the results from this observational study need to be interpreted with caution and will require confirmation by randomized clinical trials stratifying treatment groups based on MCI status at baseline.

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