Cognitive symptoms after coronavirus disease 2019 (Covid-19), the disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), are well-recognized. Whether objectively measurable cognitive deficits exist and how long they persist are unclear.
METHODS
We invited 800,000 adults in a study in England to complete an online assessment of cognitive function. We estimated a global cognitive score across eight tasks. We hypothesized that participants with persistent symptoms (lasting ≥12 weeks) after infection onset would have objectively measurable global cognitive deficits and that impairments in executive functioning and memory would be observed in such participants, especially in those who reported recent poor memory or difficulty thinking or concentrating (“brain fog”).
RESULTS
Of the 141,583 participants who started the online cognitive assessment, 112,964 completed it. In a multiple regression analysis, participants who had recovered from Covid-19 in whom symptoms had resolved in less than 4 weeks or at least 12 weeks had similar small deficits in global cognition as compared with those in the no–Covid-19 group, who had not been infected with SARS-CoV-2 or had unconfirmed infection (−0.23 SD [95% confidence interval {CI}, −0.33 to −0.13] and −0.24 SD [95% CI, −0.36 to −0.12], respectively); larger deficits as compared with the no–Covid-19 group were seen in participants with unresolved persistent symptoms (−0.42 SD; 95% CI, −0.53 to −0.31). Larger deficits were seen in participants who had SARS-CoV-2 infection during periods in which the original virus or the B.1.1.7 variant was predominant than in those infected with later variants (e.g., −0.17 SD for the B.1.1.7 variant vs. the B.1.1.529 variant; 95% CI, −0.20 to −0.13) and in participants who had been hospitalized than in those who had not been hospitalized (e.g., intensive care unit admission, −0.35 SD; 95% CI, −0.49 to −0.20). Results of the analyses were similar to those of propensity-score–matching analyses. In a comparison of the group that had unresolved persistent symptoms with the no–Covid-19 group, memory, reasoning, and executive function tasks were associated with the largest deficits (−0.33 to −0.20 SD); these tasks correlated weakly with recent symptoms, including poor memory and brain fog. No adverse events were reported.
CONCLUSIONS
Participants with resolved persistent symptoms after Covid-19 had objectively measured cognitive function similar to that in participants with shorter-duration symptoms, although short-duration Covid-19 was still associated with small cognitive deficits after recovery. Longer-term persistence of cognitive deficits and any clinical implications remain uncertain.
Poor memory and difficulty thinking or concentrating (commonly referred to as “brain fog”) have been implicated in syndromes occurring after coronavirus disease 2019 (Covid-19) — a situation that has led to suggestions that Covid-19 may have lasting cognitive consequences.1-7 However, objective data on cognitive performance are largely lacking, and how long such deficits may persist and which cognitive functions are most vulnerable are unclear.
In this observational study, our primary hypothesis was that there would be measurable cognitive deficits after Covid-19 that would scale with covariates of illness duration and severity. We secondarily speculated that objective impairments in executive and memory functions would be observable in persons with prolonged symptoms, especially poor memory or brain fog.8-10 We addressed these hypotheses by analyzing cognitive-task performance data9,11 that were obtained in the Real-Time Assessment of Community Transmission (REACT) cohort in England
Discussion
In this large community-based study, we found that Covid-19 was associated with longer-term objectively measurable cognitive deficits. The difference of approximately −0.2 SD in the global cognitive score in the groups of participants who had symptoms that had resolved, as compared with the no–Covid-19 group, is classified as “small” according to Cohen’s effect sizes24; this deficit would equate to a difference of −3 points on a typical IQ scale, in which 1 SD equals 15 points. Participants with unresolved persistent symptoms had a greater mean difference of approximately −0.4 SD. This downward shift was most evident at the distribution extreme,25 with a probability of task performance below the cutoff point for moderate impairment (−2 SD) that was 2.4 times as high among these participants as that in the no–Covid-19 group. ICU admission was associated with larger cognitive differences relative to the no–Covid-19 group (−0.63 SD, equivalent to a difference of −9 IQ points), with the probability of a score that was below −2 SD being 3.6 times as high as that in the no–Covid-19 group; this finding aligns with previous findings of medium-to-large-scale cognitive deficits in patients hospitalized in a critical care unit.2,26,27
Multiple findings indicated that the association between Covid-19 and cognitive deficits attenuated as the pandemic progressed. We found smaller cognitive deficits among participants who had been infected during recent variant periods than among those who had been infected with the original virus or the alpha variant. We also found a small cognitive advantage among participants who had received two or more vaccinations and a minimal effect of repeat episodes of Covid-19. Furthermore, the cognitive deficits that were observed in participants who had been infected during the first wave of the pandemic, when the original virus was predominant, coincided with peak strain on health services and a lack of proven effective treatments at that time, and the probability of hospitalization due to Covid-19 has progressively decreased over time.28 The finding that participants with resolved persistent symptoms had global cognitive deficits that were similar to those with shorter-duration symptoms suggests that persons with unresolved persistent symptoms may have some cognitive improvement once symptoms resolve.20
Our assessment comprised tasks that were designed to measure distinct aspects of cognitive performance that are associated with different brain systems.17 The memory, reasoning, and executive function (i.e., planning) tasks were among the most sensitive to Covid-19–related cognitive differences.9,10,26 We found that performance on these tasks differed according to illness duration and hospitalization. Scores on these tasks also correlated (albeit weakly) with recent poor memory or brain fog among participants with resolved symptoms and those with unresolved symptoms but not in the no–Covid-19 group — a finding that highlights the fact that although such symptoms are imprecise, they can reflect objectively measurable deficits. Poorer memory performance was characterized by equivalent reduced accuracy in immediate and delayed recognition rather than by accelerated forgetting — an observation that points to mechanisms of the medial temporal lobe, such as hippocampal neurogenesis,29,30 and functional interactions with frontoparietal attentional systems.31 Increased inflammation in the medial temporal lobe,32,33 accelerated atrophy of functionally associated regions of the brain,30,34 and disturbed functional dynamics have been reported after Covid-19.35,36
Although previous, often underpowered, studies have offered contradictory evidence for associations between mental health and cognitive deficits after Covid-19,5,37,38 our study was powered to detect small associations with high confidence. Our results confirmed associations of cognitive deficits with mood swings and fatigue but also with a variety of other symptoms. Therefore, it is likely that multiple underlying factors contribute to cognitive deficits after Covid-19. This heterogeneity is exemplified by the distinct cross-task profile of impairments in participants who had been admitted to the ICU, who also had cognitive consequences that have been associated with critical care.39
SARS-CoV-2 infection during the period when the delta variant was predominant was associated with better cognitive performance than infection during periods in which the original virus or alpha variant was predominant, a finding that is contrary to some previous findings (e.g., from clinics caring for persons with “long Covid-19” [also called “long Covid” or “post-Covid syndrome,” involving various constellations of symptoms after the acute phase of Covid-19]).40 Of note, the delta variant occurred in a highly vaccinated population. In addition, participants in our study were recruited by means of community-based random sampling, which resulted in the inclusion of persons with more asymptomatic and milder cases than would occur in hospital- or clinic-based studies but which also excluded persons with the most severe cases (e.g., those who died).
This study has certain limitations, including reliance on subjective reporting to identify persons with persistent symptoms. The relationship of our results to the literature about long Covid is complicated owing to a lack of established, defining criteria for post–Covid-19 syndromes. Consequently, we focused on symptoms that had persisted for at least 12 weeks, and we did not depend on a diagnosis of long Covid, which may require clinical assessment. In the absence of baseline cognitive data before infection, we could not assess cognitive change, and the observational nature of the data means that we could not infer causality.
Our calculation of the global cognitive score included the adjustment of raw performance scores for demographic characteristics and specific preexisting health conditions (as separate variables). Given the observational nature of the data, it is possible that some residual confounding remained. Consequently, in addition to standard regression analyses, we applied propensity-score matching23 as an alternative approach to address confounding. In analyses that closely matched selected participants on the basis of potentially confounding variables, we found a highly consistent pattern of results.
Any study that requires active participant engagement has a degree of participant self-selection bias. With regard to our study, persons with the most severe impairment may not have been able or willing to undertake a cognitive assessment. In addition, certain groups, including women and White persons, were slightly overrepresented in our study sample as compared with the base population, whereas younger persons and those from areas with greater levels of multiple deprivation were underrepresented. However, the sample size in our study meant that all sectors of society were represented and contributed meaningful data to the findings.
In this observational study, we found objectively measurable cognitive deficits that may persist for a year or more after Covid-19. We also found that participants with resolved persistent symptoms had small deficits in cognitive scores, as compared with the no–Covid-19 group, that were similar to those in participants with shorter-duration illness. Early periods of the pandemic, longer illness duration, and hospitalization had the strongest associations with global cognitive deficits. The implications of longer-term persistence of cognitive deficits and their clinical relevance remain unclear and warrant ongoing surveillance.
Summary: A new study uncovered a crucial link between breathing and the consolidation of memories during sleep.
Through a detailed analysis of EEG and respiratory patterns in human participants, the researchers discovered that peaks in inhalation are closely associated with an increase in slow oscillations and spindle activity in the brain. These specific brain rhythms are known to play a critical role in the process of memory consolidation.
This pivotal finding emphasizes the significant role of respiration in modulating brain activity during sleep. It opens up new avenues for understanding the complex mechanisms underlying sleep-related memory processes and disorders, potentially reshaping our approach to improving cognitive health and treating sleep-related memory impairments.
Key Facts:
The study demonstrates that respiration significantly influences the emergence of slow oscillations and spindles during sleep, two key brain rhythms involved in memory consolidation.
The strength of the coupling between respiration and these sleep oscillations correlates with the extent of memory reactivation, indicating a functional link between breathing patterns and memory processing during sleep.
The research provides evidence for the role of breathing as a potential underlying pacemaker orchestrating sleep-related brain rhythms, opening new avenues for understanding and enhancing memory consolidation during sleep.
Source: Neuroscience News
Sleep, often seen as a passive state, is a hive of brain activity where vital processes for our well-being and cognitive functions take place. One such process is memory consolidation – the transformation of experiences into lasting memories.
Recent research has taken a significant leap in understanding this phenomenon, revealing an intricate dance between our breathing and brain rhythms during sleep.
For decades, scientists have known that certain brain wave patterns during non-rapid eye movement (NREM) sleep, particularly slow oscillations and spindles, are essential for memory consolidation. However, a groundbreaking study has now established a direct link between these brain rhythms and respiration.
This study represents a paradigm shift in sleep science. It challenges existing models of memory consolidation by introducing an entirely new factor – breathing.
The study in question re-analyzed data from 20 participants, where both scalp electroencephalography (EEG) and respiration were recorded as participants learned associative memories before taking a nap. This analysis has opened a new window into our understanding of the sleep-memory nexus, particularly the role of breathing in this intricate process.
The Interplay of Breath and Brain
The researchers found that the emergence of slow oscillations and spindles – key players in memory processing – is modulated by respiration during sleep. Specifically, these brain rhythms increased around the peaks of inhalation. This modulation suggests that our breathing pattern could be acting as a conductor, orchestrating the brain’s memory consolidation process.
Memory Consolidation: A Respiration-Driven Process?
The study went a step further to link these findings to memory reactivation. The strength of the coupling between respiration and the brain’s oscillatory activities correlated with the extent of memory reactivation. Simply put, the better the coordination between breathing and brain waves, the more effective the memory consolidation.
Implications for Neuroscience and Beyond
These findings are revolutionary, not just for our basic understanding of sleep and memory but also for potential therapeutic applications. They suggest that modulating breathing patterns could be a new frontier for enhancing memory consolidation during sleep. This could have profound implications for conditions like sleep apnea, where disrupted breathing might be impairing memory processes.
The Methodology: A Fusion of Technologies
The study’s methodology, combining EEG and respiratory recordings, was crucial in uncovering these insights. By re-analyzing existing datasets with a fresh perspective on the interplay between respiration and brain waves, the researchers could unravel a hidden layer of the sleep-memory relationship.
Bridging the Gap in Sleep Research
This research bridges a significant gap in our understanding of sleep-related memory consolidation. Previous studies have highlighted the importance of slow oscillations and spindles but did not clarify what governs their occurrence. The discovery of respiration’s role provides a missing piece in this complex puzzle.
Beyond the Brain: A Holistic View
The study underscores a holistic view of bodily functions, showing how processes like breathing, often considered in isolation, are deeply intertwined with cognitive functions. This perspective opens new avenues in neuroscience, emphasizing the need to consider the body as a whole in understanding brain functions.
Future Directions: From Research to Applications
Looking ahead, this research paves the way for innovative sleep therapies aimed at enhancing memory. It also raises questions about the impact of breathing disorders on cognitive health and memory, potentially leading to new treatments for such conditions.
Challenges and Limitations
While the study is a significant step forward, it is not without limitations. The sample size was relatively small, and the study design was correlational, making it difficult to infer causation. Future research with larger and more diverse samples, perhaps using interventions to alter breathing patterns, could provide more definitive answers.
A New Paradigm in Sleep Science
This study represents a paradigm shift in sleep science. It challenges existing models of memory consolidation by introducing an entirely new factor – breathing. As we continue to unravel the mysteries of sleep, this research points us toward a more integrated understanding of how our bodies and brains work together in this fundamental state.
Conclusion
In conclusion, the discovery of breathing’s role in memory consolidation during sleep marks a significant advance in our understanding of the sleep-memory connection. It opens new pathways for research and potential therapies, bringing us closer to unlocking the full potential of our sleep for cognitive health and well-being.
Looking Ahead
As science continues to explore this fascinating connection, the dream of enhancing memory consolidation through controlled breathing during sleep inches closer to reality. This study not only expands our knowledge of sleep’s complexities but also reminds us of the wonders that lie within the most ordinary aspects of our daily lives – like taking a breath.
Abstract
Respiration modulates sleep oscillations and memory reactivation in humans
The beneficial effect of sleep on memory consolidation relies on the precise interplay of slow oscillations and spindles. However, whether these rhythms are orchestrated by an underlying pacemaker has remained elusive.
Here, we tested the relationship between respiration, which has been shown to impact brain rhythms and cognition during wake, sleep-related oscillations and memory reactivation in humans.
We re-analysed an existing dataset, where scalp electroencephalography and respiration were recorded throughout an experiment in which participants (N = 20) acquired associative memories before taking a nap. Our results reveal that respiration modulates the emergence of sleep oscillations.
Specifically, slow oscillations, spindles as well as their interplay (i.e., slow-oscillation_spindle complexes) systematically increase towards inhalation peaks. Moreover, the strength of respiration – slow-oscillation_spindle coupling is linked to the extent of memory reactivation (i.e., classifier evidence in favour of the previously learned stimulus category) during slow-oscillation_spindles.
Our results identify a clear association between respiration and memory consolidation in humans and highlight the role of brain-body interactions during sleep.
Researchers say the quality of sleep in younger years can impact memory in older age. Maria Korneeva/Getty Images
Sleep disruptions – waking up and then going back to sleep during the night – may contribute to memory and cognitive problems.
The duration of sleep was not considered in the study.
Researchers reported that cognitive issues showed up 10 years after the end of the study.
People who experience disrupted sleep in their 30s and 40s are more likely to have memory and cognitive problems later in life, according to a study published in Neurology, the journal of the American Academy of Neurology.
Researchers looked at the sleep patterns of 526 people who were followed for 11 years.
To calculate averages, the participants wore a wrist monitor for three consecutive days, one year apart. They also reported bedtimes and wake times in a sleep diary.
In addition, the partcipants completed a sleep quality survey, receiving a score ranging from 0 to 21, with higher scores indicating poorer sleep quality.
The scientists also recorded how long each person slept each night.
Participants also completed a series of memory and thinking tests.
The study included 526 participants with an average age of 40 at baseline who were followed for 11 years. Of these, 239 people, or 46%, reported poor sleep, which was defined as having a sleep score of greater than 5.
The percentage of time not moving for one minute or less
The scientists added the two percentages to determine an average sleep fragmentation score. Overall, the participants had an average sleep fragmentation score of 19%. The researchers then grouped the participants based on their scores.
The researchers reported that of the 175 participants with the most disrupted sleep, 44 had poor cognitive performance 10 years after the study ended, compared to 10 of the 176 with the least disruptive sleep.
The scientists noted that after adjusting for age, gender, race, and education, the people with the most disruptive sleep were more than twice as likely to have poor cognitive performance as those with the least disruptive sleep.
They also found no differences in cognitive performance in the middle group compared to those with the least disruptive sleep.
The length of time people slept and self-reported sleep quality were not associated with cognition in middle age.
“This important work shows how healthy brain aging is a lifelong endeavor,” says Dr. David Merrill, a geriatric psychiatrist and director of the Pacific Neuroscience Institute’s Pacific Brain Health Center in California who was not involved in the study.
“Even in early adulthood, sleep quality results in measurable changes in cognitive performance by mid-life. The study findings support the importance of sleep quality, uninterrupted, or unfragmented sleep in relation to cognitive performance,” Merrill told Medical News Today.
“Undoubtedly, we need a certain minimal quantity of sleep too, but the study wasn’t a sleep lab study, so it wasn’t structured to ask that question,” Merrill added. “Perhaps [discussing sleep patterns with my patients and] encouraging them to use sleep trackers so they can see for themselves how better sleep quality relates to days with improved energy and thinking. There are great direct-to-consumer wearables now that can allow us to know how well we’re doing to get a good quality night’s sleep.”
The researchers reported that the most significant limitation of the study was its small sample size. This prevented the researchers from thoroughly investigating potential race or gender differences.
“This is a very interesting study,” said Dr. Steven Feinsilver, the director of the Center for Sleep Medicine at Northwell Lenox Hill Hospital in New York who was not involved in the study.
“We all know that sleep is good for you and the results of this study are undoubtedly true. But the question is, what came first: Did poor sleep quality cause cognitive dysfunction or did cognitive dysfunction cause poor sleep quality?,” Feinsilver asked.
“Everyone wakes up during the night, but most people don’t remember. We have what is called retrograde amnesia – the last few minutes before falling asleep doesn’t make it into our long-term memory,” Feinsilver told Medical News Today. “This is also true of waking during the night. If we wake up and quickly go back to sleep – which is very common – we don’t remember it.”
“There is still a lot that we don’t know about sleep,” he added. “But the most important aspect is – how do you feel the next day? If you typically feel good during the day, you probably get enough sleep. The average person needs about 7.25 hours, but this is an average. Some may need more; some may need less. People aren’t very good at assessing their own sleep, but they can assess how they feel during the day.”
It is possible that cognitive function is related more to the quality of sleep rather than the length of time spent sleeping.
A studyTrusted Source completed in 2021 at Washington University Sleep Medicine Center reported that there could potentially be a middle range where cognitive function remained steady.
The scientists found that too little and too much sleep could contribute to cognitive difficulties. Cognitive scores declined in participants who slept less than 4.5 hours or more than 6.5 hours. The association held true even after adjusting for a variety of factors, including age, sex, and levels of Alzheimer’s proteins.
People who wake up feeling rested should not feel compelled to change their sleep habits, experts say.
However, those who do not sleep well might notice they have more difficulty with cognitive tasks. Treating the issue can potentially improve cognition.
Summary: Active compounds in the edible Lion’s Mane mushroom can help promote neurogenesis and enhance memory, a new study reports. Preclinical trials report the compound had a significant impact on neural growth and improved memory formation. Researchers say the compound could have clinical applications in treating and preventing neurodegenerative disorders such as Alzheimer’s disease.
Source: University of Queensland
Researchers from The University of Queensland have discovered the active compound from an edible mushroom that boosts nerve growth and enhances memory.
Professor Frederic Meunier from the Queensland Brain Institute said the team had identified new active compounds from the mushroom, Hericium erinaceus.
“Extracts from these so-called ‘lion’s mane’ mushrooms have been used in traditional medicine in Asian countries for centuries, but we wanted to scientifically determine their potential effect on brain cells,” Professor Meunier said.
“Pre-clinical testing found the lion’s mane mushroom had a significant impact on the growth of brain cells and improving memory.
“Laboratory tests measured the neurotrophic effects of compounds isolated from Hericium erinaceus on cultured brain cells, and surprisingly we found that the active compounds promote neuron projections, extending and connecting to other neurons.
“Using super-resolution microscopy, we found the mushroom extract and its active components largely increase the size of growth cones, which are particularly important for brain cells to sense their environment and establish new connections with other neurons in the brain.”
Researchers found lion’s mane mushroom improved brain cell growth and memory in pre-clinical trials. Credit: University of Queensland
Co-author, UQ’s Dr Ramon Martinez-Marmol said the discovery had applications that could treat and protect against neurodegenerative cognitive disorders such as Alzheimer’s disease.
“Our idea was to identify bioactive compounds from natural sources that could reach the brain and regulate the growth of neurons, resulting in improved memory formation,” Dr Martinez-Marmol said.
Dr Dae Hee Lee from CNGBio Co, which has supported and collaborated on the research project, said the properties of lion’s mane mushrooms had been used to treat ailments and maintain health in traditional Chinese medicine since antiquity.
“This important research is unravelling the molecular mechanism of lion’s mane mushroom compounds and their effects on brain function, particularly memory,” Dr Lee said.
The study was published in the Journal of Neurochemistry.
UQ acknowledges the collaborative efforts of researchers from the Republic of Korea’s Gachon University and Chungbuk National University.
Abstract
Hericerin derivatives activates a pan-neurotrophic pathway in central hippocampal neurons converging to ERK1/2 signaling enhancing spatial memory
The traditional medicinal mushroom Hericium erinaceus is known for enhancing peripheral nerve regeneration through targeting nerve growth factor (NGF) neurotrophic activity.
Here, we purified and identified biologically new active compounds from H. erinaceus, based on their ability to promote neurite outgrowth in hippocampal neurons. N-de phenylethyl isohericerin (NDPIH), an isoindoline compound from this mushroom, together with its hydrophobic derivative hericene A, were highly potent in promoting extensive axon outgrowth and neurite branching in cultured hippocampal neurons even in the absence of serum, demonstrating potent neurotrophic activity.
Pharmacological inhibition of tropomyosin receptor kinase B (TrkB) by ANA-12 only partly prevented the NDPIH-induced neurotrophic activity, suggesting a potential link with BDNF signaling. However, we found that NDPIH activated ERK1/2 signaling in the absence of TrkB in HEK-293T cells, an effect that was not sensitive to ANA-12 in the presence of TrkB.
Our results demonstrate that NDPIH acts via a complementary neurotrophic pathway independent of TrkB with converging downstream ERK1/2 activation. Mice fed with H. erinaceus crude extract and hericene A also exhibited increased neurotrophin expression and downstream signaling, resulting in significantly enhanced hippocampal memory.
Hericene A therefore acts through a novel pan-neurotrophic signaling pathway, leading to improved cognitive performance.
People taking statins were compared with nonusers of lipid-lowering drugs (LLDs) and users of non-statin LLDs to assess the association between statin use and memory impairment. A strong association was seen between initial statin use and diagnosis of acute memory loss within 30 days when compared with nonusers of LLDs but the association was not seen when comparing statin users with users of non-statin LLDs. However, there was an association seen between use of non-statin LLDs and acute memory loss when compared with controls not taking LLDs.
The results show that the use of statins and non-statin LLDs both increased the risk of acute memory loss in 30 days compared with nonuse. These results may indicate that all LLDs cause acute memory loss, or they may reflect detection bias.
This is an elegant epidemiologic analysis that addresses the ongoing concern that statins could potentially contribute to memory loss. Our view is that the conclusions of this provocative study are reassuring, consistent with those of other recent high-quality studies. The results show nothing special about statins, but rather that all lipid-lowering drugs are potentially associated with acute small amounts of memory loss in a small segment of adults. We agree with the authors’ view that the association is best explained by a “detection bias.” Patients who take statins or other lipid-lowering drugs may have more medical contact than others, giving more opportunities to report memory complaints, which can create a signal between lipid-lowering medications and memory even without a causal connection.
Therefore, when clinicians see patients with memory complaints on statin therapy, it is prudent to cast a wide net in line with the advice of the 2013 ACC/AHA guidelines: “evaluate the patient for nonstatin causes, such as exposure to other drugs, as well as for systemic and neuropsychiatric causes, in addition to the possibility of adverse effects associated with statin drug therapy.”
This retrospective study looked at new statin users in comparison with non-users and with users of non-statin lipid-lowering medications. These data from 1987 to 2013 were based on a database gathered by clinicians in the United Kingdom. It appears that patients on lipid-lowering drugs see their doctors more often and may thus report mild memory issues more often. Our group previously published a meta-analysis in theMayo Clinic Proceedings that statins tend to have a modest protective view against long-term memory problems.
ARYAN'S BLOG 
This is an elegant epidemiologic analysis that addresses the ongoing concern that statins could potentially contribute to memory loss. Our view is that the conclusions of this provocative study are reassuring, consistent with those of other recent high-quality studies. The results show nothing special about statins, but rather that all lipid-lowering drugs are potentially associated with acute small amounts of memory loss in a small segment of adults. We agree with the authors’ view that the association is best explained by a “detection bias.” Patients who take statins or other lipid-lowering drugs may have more medical contact than others, giving more opportunities to report memory complaints, which can create a signal between lipid-lowering medications and memory even without a causal connection.
Therefore, when clinicians see patients with memory complaints on statin therapy, it is prudent to cast a wide net in line with the advice of the 2013 ACC/AHA guidelines: “evaluate the patient for nonstatin causes, such as exposure to other drugs, as well as for systemic and neuropsychiatric causes, in addition to the possibility of adverse effects associated with statin drug therapy.”
This retrospective study looked at new statin users in comparison with non-users and with users of non-statin lipid-lowering medications. These data from 1987 to 2013 were based on a database gathered by clinicians in the United Kingdom. It appears that patients on lipid-lowering drugs see their doctors more often and may thus report mild memory issues more often. Our group previously published a meta-analysis in theMayo Clinic Proceedings that statins tend to have a modest protective view against long-term memory problems.