Is there any literature around late statin initiation and cognitive impairment? Is there literature to support early initiation of statins to decrease the risk of dementia?

Comment by InpharmD Researcher

There is limited evidence on whether the timing of statin initiation influences cognitive outcomes. Available evidence suggests that statin use may be associated with lower risk of dementia and Alzheimer’s disease, and one subgroup analysis reported stronger associations in participants younger than 70 years. One study noted that elevated lipid levels in midlife are frequently linked to a higher likelihood of cognitive decline in later years, which may add biological plausibility to the concept of earlier intervention. Evidence focused on late-life initiation shows no meaningful reduction in cognitive decline over typical follow-up periods. Societal guidelines also report that in general, statin therapy is not linked to cognitive impairment or dementia in older adults.

Background

The American Heart Association (AHA) published a 2019 evidence-based statement for the safety and tolerability of statin use. Statins are associated with rare reports of cognitive impairment based on postmarketing data. These reports were generally non-serious and reversible which resulted in loss of memory, confusion, and other forms of impairment. Two clinical trials were highlighted (HPS and PROSPER) which assessed cognitive function from simvastatin 40 mg (5 years) or pravastatin 40 mg (3 years) vs placebo in their respective studies. The results suggest similar rates of cognitive impairment. Several reviews of clinical data also report mixed results whether there is a cognitive benefit or harm from statin therapy. Based on these findings, the AHA suggests there is no definitive evidence regarding the risk of statins and cognitive decline, among other central nervous system disorders. The panel did not address whether starting statins later in life affects cognitive risk or whether earlier initiation may reduce the likelihood of developing dementia. [1]

A 2023 scientific statement from the AHA also evaluates contemporary evidence regarding the effects of aggressive LDL-C lowering on the brain, specifically its impact on dementia. The statement highlights that despite some earlier studies suggesting potential cognitive impairment associated with statins, extensive analysis of RCTs and observational data does not substantiate these concerns. Instead, the data predominantly indicate no significant adverse cognitive effects linked to aggressive LDL-C reduction over the trial durations, which range from a median of 1.6 to 6.0 years. Similar to other guidelines, the panel did not address the impact of statin initiation timing on cognitive outcomes or dementia risk. [2]

A systematic review and meta-analysis published in 2025 examined the association between statin use and the incidence of dementia and Alzheimer’s disease (AD). The research synthesized data from 42 cohort studies encompassing a total of 6,325,740 participants. The findings revealed a significant association wherein statin use resulted in a 21% reduced risk of dementia (hazard ratio [HR] 0.79, 95% confidence interval [CI] 0.71 to 0.88) and a 29% decreased risk of AD (HR 0.71; 95% CI 0.60 to 0.85). Subgroup analyses revealed that statins are more effective in preventing dementia and AD in participants with a mean/median age under 70 years compared to those over 70 years. Specifically, the HR for dementia prevention in younger participants was 0.67 (95% CI 0.56 to 0.81) versus 0.86 (95% CI 0.78 to 0.95) in older participants (p= 0.02). For AD prevention, the HR was 0.47 (95% CI 0.44 to 0.50) in the younger group compared to 0.81 (95% CI 0.71 to 0.92) in the older group (p= 0.01). No significant differences emerged from stratified analyses based on sex, geographical territory, or the lipophilicity of statins. Despite significant heterogeneity across the studies, an overarching pattern suggested greater efficacy with higher statin dosages and extended exposure durations. Sensitivity analyses confirmed the robustness of these outcomes, especially under different diagnostic criteria for dementia/AD. The meta-analysis underscored the implications of the findings for clinical practice, particularly highlighting the importance of early initiation and sustained use of statins among younger populations to maximize cognitive protection. [3]

A 2025 narrative review examines the complex relationship between statin use and cognitive health. This review highlights the ongoing debates regarding whether statins confer neuroprotective benefits or pose a risk of cognitive impairment, with an emphasis on examining the biochemical and physiological mechanisms at play. Statins, known for their efficacy in lowering low-density lipoprotein cholesterol (LDL-C) and preventing cardiovascular disease (CVD), are scrutinized for their potential impact on mental functions due to the distinctive cholesterol homeostasis in the brain, the blood-brain barrier’s limited permeability to lipoproteins, and the varying lipophilicity of different statin formulations. Despite a prevalent belief in possible cognitive side effects, recent epidemiological studies, as cited in the review, suggest that statins may actually offer neuroprotective benefits, though these findings are hindered by biases such as selection bias, confounding variables, and reverse causation. Two pivotal randomized controlled trials, STAREE and PREVENTABLE, are currently underway and anticipated to fill gaps in the literature by providing rigorous, objective analyses of statins’ effects on cognition. Existing literature reveals mixed results, with early studies indicating potential cognitive disturbances associated with statin use, while more recent large-scale studies have failed to substantiate these concerns. Observational data, particularly from large cohorts, have suggested that statins may be linked to a reduced incidence of Alzheimer’s disease and other forms of dementia, although methodological limitations necessitate caution in interpreting these findings. The review underscores the need for further well-designed trials to elucidate the differential impacts of statin type, dose, and treatment duration on cognitive outcomes, as well as their effects on individuals with mild cognitive impairment, diabetes, chronic kidney disease, and other high-risk conditions. [4]

A 2015 systematic review evaluated RCTs and observational studies assessing whether statin use influences cognitive outcomes. Evidence summarized in the review indicates that initiation of statins in late life does not prevent cognitive decline or dementia over the subsequent 3 to 5 years. The authors also note that the current literature does not address whether mid-life or long-term statin use has beneficial cognitive effects, leaving uncertainty regarding potential advantages of earlier initiation. Although several observational studies that used time-updated statin exposure reported an apparent protective association, the review concludes that these findings are likely attributable to reverse causation, given that developing cognitive impairment can reduce adherence to or likelihood of statin prescribing. Overall, the review emphasizes that existing evidence does not support starting statins in late life to prevent cognitive decline, and that whether earlier initiation reduces dementia risk remains unaddressed by available studies. [5]

A 2019 poster abstract examined the complex interplay between lipid profiles, statin use, and cognitive function. This review included publications evaluating associations between cholesterol levels and/or statin use and cognition, focusing on both male and female subjects aged 45 and over. Among studies assessing cholesterol levels and cognition, a predominant number (n=21) indicated that elevated lipid profiles during midlife significantly heightened the risk of developing dementia and cognitive decline in later years (mean age <70 years). Conversely, 17 studies suggested that higher cholesterol levels could positively affect cognition in individuals aged over 70. Furthermore, 16 studies highlighted a link between higher HDL levels and improved cognitive function, alongside a protective role against dementia, while four studies found no association and one observed a potential connection between high HDL and increased neuritic plaques. In contrast, seven studies showed no correlation between cholesterol levels and cognitive performance. In a similar vein, the examination of statin use and cognitive outcomes yielded mixed results. Among the studies reviewed, seven demonstrated a lower risk of cognitive decline for statin users, whereas 23 studies reported potential negative effects of statins on cognition. Additionally, 18 studies did not find any significant association between statin use and cognitive decline. Overall, the results from studies assessing both lipid profiles and statin use underscore the need for more extensive longitudinal research to elucidate these relationships further. Notably, the follow-up duration in most statin-related studies did not exceed five years, leaving the long-term cognitive effects of statin use uncertain. Therefore, it is imperative to undertake additional longitudinal studies investigating the prolonged impact of statin therapy on cognitive decline, particularly spanning from mid to late life. [6]

References:

[1] Newman CB, Preiss D, Tobert JA, et al. Statin Safety and Associated Adverse Events: A Scientific Statement From the American Heart Association. Arterioscler Thromb Vasc Biol. 2019;39(2):e38-e81. doi:10.1161/ATV.0000000000000073
[2] Goldstein LB, Toth PP, Dearborn-Tomazos JL, et al. Aggressive LDL-C Lowering and the Brain: Impact on Risk for Dementia and Hemorrhagic Stroke: A Scientific Statement From the American Heart Association. Arterioscler Thromb Vasc Biol. 2023;43(10):e404-e442. doi:10.1161/ATV.0000000000000164
[3] Du Y, Yu Z, Li C, Zhang Y, Xu B. The role of statins in dementia or Alzheimer's disease incidence: a systematic review and meta-analysis of cohort studies. Front Pharmacol. 2025;16:1473796. Published 2025 Feb 3. doi:10.3389/fphar.2025.1473796
[4] Kazibwe R, Rikhi R, Mirzai S, Ashburn NP, Schaich CL, Shapiro M. Do Statins Affect Cognitive Health? A Narrative Review and Critical Analysis of the Evidence. Curr Atheroscler Rep. 2024;27(1):2. Published 2024 Nov 9. doi:10.1007/s11883-024-01255-x
[5] Power MC, Weuve J, Sharrett AR, Blacker D, Gottesman RF. Statins, cognition, and dementia—systematic review and methodological commentary. Nat Rev Neurol. 2015;11(4):220-229. doi:10.1038/nrneurol.2015.35
[6] Chin TJ, Gorelik A, Szoeke C, Goonewardena K. P3‐299: association between lipids, statin and cognition: is timing the key? Alzheimer’s & Dementia. 2019;15(7S_Part_20). doi:10.1016/j.jalz.2019.06.3330

Literature Review

A search of the published medical literature revealed 2 studies investigating the researchable question:

Is there any literature around late statin initiation and cognitive impairment? Is there literature to support early initiation of statins to decrease the risk of dementia?

Level of evidence

C - Multiple studies with limitations or conflicting results  Read more→



Please see Tables 1-2 for your response.


Statin Initiation and Dementia Incidence in a Large Health Care System From 1997 to 2020: A Target Trial Emulation Study

Design

Cohort study emulating a target trial using data from Kaiser Permanente Northern California (KPNC)

N= 705,061

Objective

To estimate the association between the first statin prescription and incident Alzheimer's disease and Alzheimer's disease-related dementias (AD/ADRD) among members of a large population-based cohort of older adults

Study Groups

Statin initiators (n= 264,294)

Noninitiators (n= 255,937)

Inclusion Criteria

Participants born before 1951 and KPNC members for 4+ years during 1997–2010

Exclusion Criteria

Participants with extreme propensity scores, those dispensed statins, diagnosed with AD/ADRD, or had no laboratory tests or dispensing records during the run-in period

Methods

Participants initiating a statin between 2001–2010 were matched to five noninitiators on age (±5 years) and LDL-C category (<70, 70–99, 100–129, 130–159, 160–189, ≥190 mg/dL). Follow-up began at the date of first statin prescription for initiators and the matched date for noninitiators.

Covariates were obtained from EHR up to baseline, including comorbidities, demographics, LDL-C, HDL-C, HbA1c, and health care utilization metrics. Missing labs were imputed using sample means within disease strata.

Statin exposure was intent-to-treat. Cox proportional hazards models were used, adjusted for age, LDL-C, propensity score deciles, and stabilized IPTWs. Analyses estimated hazard ratios separately for the first year after initiation and subsequent years.

Duration

January 1, 1997, to December 31, 2020

Outcome Measures

Primary: Time to incident AD/ADRD diagnosis

Secondary: Time to diagnosis of Alzheimer's disease (AD)

Baseline Characteristics  

Statin initiators (n= 264,294)

Noninitiators (n= 255,937)
Mean age at baseline, years

67.4

67.4
Female

55.1%

55.1%
Follow-up time, years

11.8

11.8
Results

In the full EHR cohort, statin initiation was associated with a transient increase in dementia diagnoses during the first year of follow-up, with fully adjusted hazard ratios of 1.46 (95% CI, 1.42–1.53) for AD/ADRD and 1.35 (95% CI 1.24–1.50) for Alzheimer's disease alone.

This short-term elevation is consistent with heightened medical contact or diagnostic surveillance rather than a pharmacologic effect. Beyond the first year, statin initiation showed no meaningful association with dementia risk: the hazard ratio for AD/ADRD was 1.00 (95% CI 0.99–1.01), and for Alzheimer's disease was 1.03 (95% CI 1.01–1.06), indicating essentially null long-term effects.

Overall, the findings suggest that while diagnostic rates temporarily rise immediately after statin initiation, long-term dementia incidence does not differ between statin initiators and matched noninitiators.

Adverse Events

Not applicable.

Study Author Conclusions

AD/ADRD diagnoses increased transiently in the first year after statin initiation, likely attributable to factors other than statin use per se. After the first year, initiation of statins was not associated with AD/ADRD diagnoses in this large and diverse cohort over extended follow-up.

Critique

The study's large sample size and long follow-up period are strengths, allowing for robust analysis of statin initiation effects. However, the observational design may still be subject to residual confounding, and the intent-to-treat analysis does not quantify effects of long-term statin exposure. The study's reliance on clinical diagnoses may introduce misclassification bias, although this is mitigated by the integrated health system setting.

 

References:

Zimmerman SC, Choi M, Jiang C, et al. Statin Initiation and Dementia Incidence in a Large Health Care System From 1997 to 2020: A Target Trial Emulation Study. Neurology. 2025;105(2):e213855. doi:10.1212/WNL.0000000000213855

Statins, Risk of Dementia and Cognitive Function: Secondary Analysis of the Ginkgo Evaluation of Memory Study (GEMS)
Design

Longitudinal, observational study

N= 3,069

Objective To examine whether 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
Study Groups

No MCI at baseline (n= 2,587)

MCI at baseline (n= 482)

Inclusion Criteria Patients ≥75 years, cognitively healthy or with mild cognitive impairment (MCI)
Exclusion Criteria Individuals unable to sign informed consent or without a proxy to provide an independent assessment of functional and cognitive abilities
Methods

Participants underwent detailed physical, neurological, and neuropsychiatric examinations. Medical history and LLM use were assessed at baseline and every 6 months. Participants brought their medicine bottles to the clinic to record the exact name and dose of each. Fasting lipid profiles were not measured.

At each follow-up visit, cognitive function was evaluated using the Modified Mini-Mental State Exam (3MSE), the Clinical Dementia Rating Scale, and the cognitive subscale of the Alzheimer's Dementia Assessment Scale (ADAS-Cog). Individuals who reached the dementia endpoint were excluded from further assessments.

Duration Mean follow-up: 6 years
Outcome Measures

Primary: Time to adjudicated all-cause dementia and Alzheimer's Dementia (AD)

Secondary: Change in global cognitive function over time (measured by 3MSE and ADAS-cog scores)

Baseline Characteristics   No LLM (n= 2218) Statins (n= 778) Other LLM (n= 73) p-value
Age, years 78.7 ± 3.4 78.4 ± 3.0 77.8 ± 2.9 0.007
Female 48.3% 41.3% 37% 0.001
Race - Black 3.2% 2.4% 0% 0.18
MCI 15.6% 15.8% 17.8% 0.87
Cerebrovascular disease 6.6% 13.5% 6.8% <0.001
Coronary heart disease 9.9% 47.6% 34.2% <0.001
Education, years 14.3 ± 3.2 14.5 ± 3.1 14.8 ± 3.2 0.26
3MSE 93.4 ± 4.7 93.2 ± 4.6 93.7 ± 4.7 0.34
ADAS-cog 6.5 ± 2.7 6.5 ± 2.7 6.3 ± 2.4 0.86

At baseline, 25.3% of participants were taking statins, and 2.4% were taking other LLMs, including bile-acid sequestrants, fibrates, niacin, or nicotinic acid.

Abbreviations: 3MSE= Modified Mini-Mental State Exam. ADAS-cog= cognitive subscale of the Alzheimer's Dementia Assessment Scale. MCI= mild cognitive impairment.

Results   No MCI at baseline  MCI at baseline p-Value

Change in 3MSE score, points/yeara

-0.09 (-0.13 to -0.06) -0.45 (-0.58 to -0.32) -
Change in ADAS-cog score, points/yeara 0.03 (0.01 to 0.05) 0.18 (0.12 to 0.24) -

There was a reduction in risk of AD and all-cause dementia among those who initiated statin use during the study (HR 0.46; 95% CI 0.29 to 0.74, p< 0.001), and (HR 0.53; 95% CI 0.37 to 0.75, p< 0.001), respectively.

Among participants without MCI at baseline, current use of statins was consistently associated with a reduced risk of all-cause dementia (HR 0.79; 95% CI 0.65 to 0.96, p= 0.021) and AD (HR 0.57; 95% CI 0.39 to 0.85, p= 0.005).

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.

a. Linear rate of change at the 3rd year of follow-up.

Abbreviations: 3MSE= Modified Mini-Mental State Exam. AD= Alzheimer's Dementia. ADAS-cog= cognitive subscale of the Alzheimer's Dementia Assessment Scale. CI= confidence interval. HR= hazard ratio. MCI= mild cognitive impairment.

Adverse Events Not specified.
Study Author Conclusions Statins reduce the risk of incident AD and all-cause dementia in elderly individuals without MCI at baseline. However, confirmation of these results by randomized trials stratifying participants by MCI status would be required.
Critique The study's strengths include a large sample size and regular cognitive assessments over an extended period. However, limitations include the observational design, lack of cholesterol level measurements, and potential confounding by indication. The study's findings need confirmation through randomized controlled trials to establish causality and address potential biases.

 

References:

Bettermann K, Arnold AM, Williamson J, et al. Statins, risk of dementia, and cognitive function: secondary analysis of the ginkgo evaluation of memory study. J Stroke Cerebrovasc Dis. 2012;21(6):436-444. doi:10.1016/j.jstrokecerebrovasdis.2010.11.002