Evidence for the efficacy of piracetam for dementia or cognitive impairment is inadequate for clinical use but sufficient to justify further research

Piracetam was one of the first drugs used for dementia and comes from the class of drugs called nootropics, whose putative actions are still poorly defined. Most of the trials of piracetam were undertaken many years ago and did not use methods which would be currently considered standard. Some of the studies suggested there may be some benefit from piracetam but overall the evidence is not consistent or positive enough to support its use for dementia or cognitive impairment.

Authors' conclusions: 

Published evidence does not support the use of piracetam in the treatment of people with dementia or cognitive impairment. Although effects were found on global impression of change, no benefit was shown by any of the more specific measures of cognitive function.

The evidence indicates a need for further evaluation of piracetam.

Read the full abstract...

Piracetam is a drug that may enhance memory and other intellectual functions, but its usefulness in treating dementia is uncertain. It is, however, commonly prescribed for cognitive impairment and dementia in several countries of continental Europe.


To determine the clinical efficacy of piracetam for features of dementia (classified into the major subtypes: vascular, Alzheimer's disease or mixed vascular and Alzheimer's disease, or unclassified dementia) or cognitive impairment not fulfilling diagnostic criteria for dementia.

Search strategy: 

We searched ALOIS - the Cochrane Dementia and Cognitive Improvement Group’s Specialized Register on 4 December 2011 using the terms: piracetam, nootropic, "2-Oxo-1-pyrrolidine", Lucetam, Nootropil, Breinox. We identified another review by employees and consultants of the manufacturing company, UCB Pharma (Waegemans 2002) which included data from unpublished studies not made available to Cochrane review authors.

Selection criteria: 

All unconfounded, randomized, double-blind trials in which treatment with piracetam was administered for more than a day and compared with placebo in people with dementia of Alzheimer type, vascular dementia, or mixed vascular and Alzheimer's disease, or unclassified dementia, or cognitive impairment not fulfilling diagnostic criteria for dementia.

Data collection and analysis: 

Two review authors independently extracted data from studies fulfilling the inclusion criteria. We used Intention-to-treat analysis where feasible and pooled studies if appropriate. We planned to perform sensitivity analyses to determine if studies performing poorly on quality criteria affected results. The pharmaceutical company marketing piracetam did not release the results of several unpublished trials.

Main results: 

There were 24 included studies with 11959 participants in total. Many studies were of cross-over design and first-phase data were unavailable, or could not be extracted. Global impression of change (GIC) was the only outcome for which pooling of data was possible, involving only four studies. There was evidence of heterogeneity in the results, Chi2 test = 19.17 (df = 3, P < 0.001). The odds ratio (OR) for improvement in the piracetam group compared with placebo was 3.43 (95% confidence interval (CI) 2.32 to 5.07). Using a fixed-effect model, the OR for improvement with piracetam compared with placebo was 3.55 (95% CI 2.45 to 5.16). This estimate was derived from completers rather than from an intention-to-treat analysis as relevant data could not be extracted from the reports.

In the limited data available, no significant differences were found between treatment and placebo groups for cognition (immediate memory, visuospatial, Mini Mental Status Examination (MMSE), delayed memory or speech) for dependency, or for depression.

The large volume of unpublished and untraceable data not available to the review authors raises the possibility of publication bias.