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 was characterized as a pandemic, it was clear that older adults in general, and those with 

 (ADRD) in particular, would be severely impacted both directly by the virus and indirectly by the social consequences and responses.

 Now, approaching 2 years since SARS-CoV-2 emerged, we are starting to measure the impact of COVID-19 on older patients with cognitive impairment and ADRD. Further, we can begin to review neurobiological issues associated with COVID-19 in older adults, and consider how COVID-19 may contribute to cognitive impairment and future cases of dementia.

The demographics of COVID-19 cases have shifted over time, with older adults being most impacted early in the pandemic, and later waves involving younger individuals.

 Similarly, risk varied by setting, with an early wave of COVID-19 cases in congregate settings including nursing homes, retirement homes, and hospitals. These frequent and widespread outbreaks were associated with significant morbidity and mortality. Despite campaigns to vaccinate nursing home residents, they still account for a large proportion of the total deaths due to COVID-19.

The severity of COVID-19 spans the spectrum from asymptomatic carrier state to severe illness and death, with age being the strongest demographic risk factor for a more severe illness: Age has an exponential relationship with infection fatality rate, reaching 15% at age 85.

 Older adults with cognitive impairment are doubly at risk, with age and cognitive impairment independently contributing to illness severity.

 Cognitive impairment has been associated with double the risk of COVID-19 mortality in nursing homes.

 Even when controlling for residence in a nursing home, those with dementia had twice the risk of acquiring COVID-19.

We had anticipated that rates of behavioral and psychologic symptoms associated with dementia (BPSD) would increase as a result of indirect factors such as disruption to care, social isolation, and disruption to routine.

 Unfortunately, this has been borne out, with studies reporting increases in BPSD including anxiety, depression, insomnia, wandering, and agitation.

Alongside the risk of mortality, the pandemic is also affecting mental health negatively, both via the direct effect of the virus and indirectly via the massive disruption to society in response to the pandemic. Early and ongoing mental health consequences of the pandemic include increased rates of symptoms of depression, anxiety, substance use, and suicidal ideation. However, paradoxically, younger individuals may be more impacted than older ones.

 Similarly, while the pandemic may have increased BPSD in some individuals with dementia, this has not been universally true. For example, in New Brunswick, Canada, despite a marked reduction in family visits and periods of lockdown (mitigated by virtual visits and volunteer services), there was no change in rates of agitation, and a reduction in rates of depression among nursing home residents, with more than half of them having dementia.

The availability of safe and effective COVID-19 vaccines is thought to be a key element to ending the pandemic. Early on, in the context of limited supply, governments prioritized vaccination for high-risk groups such as the elderly and those living in long-term care (LTC) facilities. Thus, most individuals with dementia were prioritized for vaccination. For example, in Ontario, Canada, despite only 0.5% of the population living in LTC facilities, vaccination initially was reserved for LTC residents and health professionals when vaccines first became available in December 2019.

 By March 2020, more than 92% of LTC residents had received at least 1 dose of a COVID-19 vaccine, which was estimated to have reduced mortality by 96%.

 The recent approval by the US Food and Drug Administration of booster shots for older persons (ie, a third dose) may offer them further protection and also deepen current inequities when vaccination remains unavailable due to supply constraints in some jurisdictions.

COVID-19 is transmitted person to person via inhalation of respiratory droplets and their deposition on mucous membranes, and to a lesser extent by contaminated hands contacting mucous membranes.

 The virus enters cells via the angiotensin-converting enzyme 2 receptor, present not only in the respiratory and gastrointestinal tract but also in other organs, including the brain and blood vessels.

 Thus, COVID-19 can potentially lead to neuropathology via systemic and inflammatory indirect effects and by its direct action on the nervous system.

Although most cases of COVID-19 are classified as mild, severe cases occur in individuals of all ages, most commonly in older adults. Common acute symptoms include cough, fever, fatigue, headache, myalgias, and diarrhea.

 Symptoms can progress and involve hypoxemia and acute respiratory distress syndrome.

 In addition, injury to all organ systems due to severe inflammation, thromboembolic events, and neurologic complications can occur.

The neurologic consequences of severe COVID-19 are common and involve both the central nervous system (CNS) and peripheral nervous system (PNS) (

 Dizziness and headache are the most common CNS manifestations, which can also include cerebrovascular disease (eg, ischemic stroke, hemorrhage), ataxia, and seizure. Delirium is a common presentation of older adults with COVID-19; it has a very poor prognosis and is associated with permanent cognitive impairment.

 Anosmia and ageusia are the most common PNS manifestations.

Neurologic manifestations can occur within the first days of illness and persist months after hospital discharge.

 Isolating the virus in cerebrospinal fluid is rare.

 Cognitive impairment is a commonly reported symptom in survivors of severe COVID-19 at 60 days post discharge.

 Although research is needed to confirm the neuropsychiatric sequelae of COVID-19, a broad spectrum of neuropsychiatric symptoms have been reported, including headaches, sleep disorders, encephalopathy, myalgia, and ageusia.

 The term long COVID refers to the persistence of symptoms after the resolution of the acute infection, and a broad range of symptoms have been reported, including neuropsychiatric symptoms such as cognitive impairment, insomnia, impaired concentration, posttraumatic symptoms, and headache.

 Long COVID is not always associated with the severity of acute COVID-19 or risk factors for severe COVID-19, and it may involve multiple organ damage by other direct mechanisms.

 Long COVID is thought to be relatively common, but estimates of its prevalence vary widely depending on definition and time since infection. It may also depend on the SARS-CoV-2 genetic variant.

There is evidence for both structural and functional brain changes following COVID-19, and these changes may be associated with the neurologic symptoms of long COVID. Various studies have reported heterogenous findings. A recent systematic review summarizing the neuroimaging findings associated with COVID-19 in older adults reported widespread neuropathological issues typically associated with cerebrovascular damage, most consistently in white matter, brainstem, and frontotemporal cortical areas.

 A case-control study of patients who recovered from COVID-19 found hypometabolism in frontotemporal regions, which was associated with neurological symptoms.

 A study of United Kingdom Biobank participants by Douaud et al found changes in 394 individuals who had brain imaging before and after a COVID-19 infection, compared with 388 matched controls without a history of COVID-19. Among those who had survived COVID-19, Douaud et al identified reductions in grey matter in the left parahippocampal gyrus, left lateral orbitofrontal cortex, and left insula.

Although it is staggering that approximately 1 in 500 Americans has died of COVID-19, mortality is the tip of the iceberg. The Centers for Disease Control and Prevention estimates that as of May 29, 2021, there had been more than 100 million individuals with symptomatic COVID-19 in the United States, 10 million of them 65 years or older.

 The sequelae from severe COVID-19 are risk factors for dementia, and they may increase the growing number of individuals living with dementia. Understanding the specific contribution of a past COVID-19 infection on future risks of dementia will require longitudinal studies. These risks may be substantial given the cerebrovascular changes associated with past infection. During the next few years, post-COVID-19 issues may occur mostly in older adults. However, COVID-19 may also increase the risk of future cognitive impairment and dementia in younger individuals, because early life experiences and exposures contribute to the risk of dementia, as is the case in other risk factors for dementia such as low level of education or depression early in life. The magnitude of the current and future human, financial, and societal cost of COVID-19 is unknown, but certainly worrisome.

On the other hand, we expect that the pandemic will lead to numerous changes that benefit older adults. Specifically, the spotlight on nursing homes has revealed systemic flaws and inequities in many countries that now will be hard to ignore. The pivot to virtual care has spurred some innovation that may facilitate access to care going forward.

In our own experience, working at the Centre for Addiction in Mental Health in Toronto, we have had to pivot to providing care to older individuals despite multiple waves of COVID-19 cases in the community. Some of the changes in our practice and our environment will have long-lasting benefits. The heterogeneity of real-world experience, compared with averages often reported in research, is humbling. Some of our older patients have shown remarkable resilience through the pandemic and have adjusted their lifestyle to thrive during this time. Others have had their usual coping mechanisms totally disrupted and are suffering, needing additional mental health and social resources. In our geriatric mental health inpatient unit, technology (eg, internet-connected tablets) has been helpful to connect patients to family, activities, and entertainment. We have also noticed an improved access to specialist consultations with virtual care and additional physician-to-physician consultation options. In our outpatient setting, virtual care options introduced to reduce risk of COVID-19 have also reduced barriers for certain patients who prefer it or may have mobility issues.

The impact of the pandemic on older adults and those with dementia has been immense. Vaccination can dramatically reduce severe outcomes from COVID-19 in older adults. The indirect impact of the pandemic on individuals with dementia, such as isolation and disruption of care, can be pronounced, but they can also be mitigated. COVID-19 causes neurological damage that is not restricted to severe cases or older adults. A significant proportion of individuals infected by COVID-19 will experience long-term negative impact, including an increased risk of dementia. Research to better understand the neurobiology and the long-term neuropsychiatric impacts of COVID-19 is critical, as it will shift the understanding of the risk-benefit of population-level interventions to prevent COVID-19. The pandemic is not over. Efforts to protect everyone, including older adults, from COVID-19 are essential.

 is an assistant professor of psychiatry at the University of Toronto and a clinician scientist at the Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, in Toronto, Canada. 

 is an associate professor of psychiatry at the University of Toronto and chief of geriatric psychiatry at the Centre for Addiction and Mental Health. 

 is the Labatt Family Chair of the Department of Psychiatry in the Faculty of Medicine at the University of Toronto and a clinician scientist in the Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health.

Anticipating and mitigating the impact of the COVID-19 pandemic on Alzheimer’s disease and related dementias

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Changing age distribution of the COVID-19 pandemic – United States, May-August 2020

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Risk factors associated with all-cause 30-day mortality in nursing home residents with COVID-19

Nursing home care in crisis in the wake of COVID-19

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Assessing the age specificity of infection fatality rates for COVID-19: systematic review, meta-analysis, and public policy implications

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Dementia is an age-independent risk factor for severity and death in COVID-19 inpatients

COVID-19 and dementia: analyses of risk, disparity, and outcomes from electronic health records in the US

Effectively caring for individuals with behavioral and psychological symptoms of dementia during the COVID-19 pandemic

9. Dellazizzo L, Léveillé N, Landry C, Dumais A. 

Systematic review on the mental health and treatment impacts of COVID-19 on neurocognitive disorders

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Follow-up survey of US adult reports of mental health, substance use, and suicidal ideation during the COVID-19 pandemic, September 2020

11. McArthur C, Saari M, Heckman GA, et al. 

Evaluating the effect of COVID-19 pandemic lockdown on long-term care residents’ mental health: a data-driven approach in New Brunswick

12. Brown KA, Stall NM, Vanniyasingam T, et al. Early impact of Ontario’s COVID-19 vaccine rollout on long-term care home residents and health care workers. Science Table: COVID-19 Advisory for Ontario. March 8, 2021. Accessed October 5, 2021. 

https://covid19-sciencetable.ca/wp-content/uploads/2021/03/Science-Brief_LTC-and-Vaccine_20210308_version-1.1_published-1.pdf

13. Scientific brief: SARS-CoV-2 transmission. Centers for Disease Control and Prevention. Updated May 7, 2021. Accessed September 28, 2021. 

https://www.cdc.gov/coronavirus/2019-ncov/science/science-briefs/sars-cov-2-transmission.html

14. Hamming I, Timens W, Bulthuis MLC, et al. 

Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. a first step in understanding SARS pathogenesis

Long Covid – mechanisms, risk factors, and management

Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China

18. Marengoni A, Zucchelli A, Grande G, et al. 

The impact of delirium on outcomes for older adults hospitalised with COVID-19

19. Chopra V, Flanders SA, O’Malley M, et al. 

Sixty-day outcomes among patients hospitalized with COVID-19

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Neurological presentations of COVID-19: findings from the Spanish Society of Neurology neuroCOVID-19 registry

21. Nalleballe K, Reddy Onteddu S, Sharma R, et al. 

Spectrum of neuropsychiatric manifestations in COVID-19

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

23. Manca R, De Marco M, Ince PG, Venneri A. 

Heterogeneity in regional damage detected by neuroimaging and neuropathological studies in older adults with COVID-19: a cognitive-neuroscience systematic review to inform the long-term impact of the virus on neurocognitive trajectories

24. Guedj E, Campion JY, Dudouet P, et al. 

F-FDG brain PET hypometabolism in patients with long COVID

25. Douaud G, Lee S, Alfaro-Almagro F, et al. 

Brain imaging before and after COVID-19 in UK Biobank

26. Estimated COVID-19 burden. Centers for Disease Control and Precention. Updated July 27, 2021. Accessed September 28, 2021. 

https://www.cdc.gov/coronavirus/2019-ncov/cases-updates/burden.html

How does COVID-19 contribute to cognitive impairment in older adults and future cases of dementia?

COVID-19, Cognition, and Dementias: What Role Has the Pandemic Played?

Financial exploitation is one of the most prevalent forms of 

 Older adults are more likely to have a “nest egg,” own their home, have excellent credit, and they are generally raised to be polite and trusting. Moreover, with age also comes reduced sensitivity to negative arousal cues, so even cognitively intact older adults can have functional changes that may render them financially vulnerable.

 Estimates by MetLife indicate that senior citizens lost $2.9 billion to elder financial abuse in 2010, and up from $2.6 billion in 2008.

The Federal Trade Commission’s survey on fraud prevalence in the United States revealed that African American and Latino consumers were more likely to become victims of fraud than non-Hispanic whites.

Given that elder financial exploitation is associated with mortality, hospitalization, poor physical and mental health, lower quality of life, loss of independence, and significant financial hardship, fighting “the crime of the 21st century” is of utmost importance. As the elderly population continues to grow and become more diverse, primary intervention strategies will benefit both elderly and minority populations.

In 2010, approximately 1 in 5 Americans aged 65 years or older fell victim to financial abuse.

 require higher-order cognitive processes that decline with age. Even cognitively intact older adults can have functional brain changes that may render them financially vulnerable. The elderly population (aged 65 and older) is projected to reach 70 million by 2030. These estimates raise concern that increased susceptibility to deception will drive reduced quality of life and loss of independence, thereby negatively impacting the health status for a large segment of the US population.

Individuals with cognitive impairment are at increased risk of becoming victims of scams due to decreased awareness, overestimation of competency in financial matters, social vulnerability, and changes in perceptual speed, episodic memory, and working memory.

 (AD) are more likely to suffer the loss of twice as much money per case of financial exploitation.

 Poor decision making and greater susceptibility to scams have also been linked to mild cognitive impairment (MCI), and these vulnerabilities can emerge even prior to a diagnosis of actual MCI.

 The prevalence of individuals with AD in the US population is growing and will increase almost threefold to 13.2 million by 2050.

 Current estimates project that 1 in every 45 Americans will have AD by 2047.

 In adults with MCI and AD, structural brain changes and deterioration in cognitive capacitates such as processing speed and episodic memory exacerbate susceptibility to scams.

 Diminished cognitive functioning has been linked not only to greater financial victimization in old age, but to AD onset as well.

The disease burden of AD is associated with weakened financial capacity and financial autonomy, thereby increasing family 

 Financial capacity is crucial for independent activities in daily life; however, individuals with AD and cognitive decline often demonstrate total loss of financial capacity, which can lead to psychological burden and distress.

 Impairments in financial capacity also contribute to economic hardship, significant concerns for patient welfare, and family caregiver burden. This is particularly important in light of a recent survey of 2000 nonprofessional caregivers which found that 92% provide financial assistance for the adults they care for.

 Managing AD patients’ disease and functional independence is an expensive endeavor, and financial exploitation only exacerbates the problem. Moreover, financial mismanagement among cognitively impaired individuals is one of the greatest sources of perceived caregiver burden.

 safeguards are crucial to protect this population and their caregivers from scams. The chronic burden associated with fighting a degenerative disease, lapses in memory and judgment, and caregiver fatigue are examples of why individuals with MCI or AD and their caregivers are vulnerable targets for “the crime of the 21st century.” The impact of financial scamming on older adults and their families has direct implications for clinical care, particularly as psychiatrists and other mental health experts may be in a prime position to identify at-risk individuals 

“Mr Xavier” is a 76-year-old gentleman recently diagnosed with MCI who receives a phone call from someone who claims to be his grandchild. The caller is frantic and explains that they are traveling abroad and have come into health troubles. They would like Mr Xavier to urgently wire money in order to settle the emergency. Specifically, the caller indicates that they require the money in order to pay a pressing hospital bill. The caller indicates just enough information to make the situation seem plausible. The caller then turns the phone over to a “doctor” who legitimizes the story. The caller seems quite embarrassed by the medical emergency and asks Mr Xavier to keep his financial assistance a secret from other family members and friends (eg, “Don’t tell mom; don’t tell dad!”).

The current best protection against scams is education for 

. As examples, the FBI, the Consumer Financial Protection Bureau, USA.gov, and AARP all provide guidance on protection from scams. The status quo, as it pertains to prevention of scamming, includes hotlines, “info-commercial” home-based online education, legal interventions, and public lectures by law enforcement officials. Although these approaches have been shown to be cost effective and provide rapid response, major limitations to these intervention methods are that they: 1) do not preemptively target populations cognitively vulnerable to deception; 2) are not holistic and do not incorporate caregivers; and 3) are not often accessible to multilingual populations. A priori screening for susceptibility to deception and educational interventions would minimize adverse health outcomes and high costs of care, and may provide crucial interventions to both patients and their caregivers.

It is paramount that interventions for scamming specifically target vulnerable populations. Practicing psychiatrists and other mental health care providers are well positioned to conduct cognitive evaluations, assess capacity for financial decision making, and advise in advance care planning such as setting up trusts or facilitating discussions about creating a durable power of attorney. A behavioral science-based primary intervention approach would facilitate overcoming barriers, thereby opening new horizons for reducing public health burden due to financial fraud.

 is an instructor in the Division of Neuropsychology, in the Department of Neurology of the University of Miami Miller School of Medicine. 

is a professor of neurology at the University of Miami Miller School of Medicine and founding director of the Comprehensive Center for Brain Health.

This study was supported by grants to SJG from the American Academy of Neurology, American Brain Foundation, and McKnight Brain Research Foundation, and to JEG from the National Institute on Aging (R01 AG071514, R01 AG069765, R01 AG057681, and R01 NS101483), the Harry T. Mangurian Foundation, and the Leo and Anne Albert Charitable Trust. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

1. Acierno R, Hernandez MA, Amstadter AB, et al. 

Prevalence and correlates of emotional, physical, sexual, and financial abuse and potential neglect in the United States: The National Elder Mistreatment Study

Decision making in the ageing brain: changes in affective and motivational circuit

3. Carstensen LL, Turan B, Scheibe S, et al. 

Emotional experience improves with age: evidence based on over 10 years of experience sampling

Social economic decision-making across the lifespan: an fMRI investigation.

5. Amstadter AB, Zajac K, Strachan M, et al. 

Prevalence and correlates of elder mistreatment in South Carolina: the South Carolina elder mistreatment study

6. Anderson KB. Consumer fraud in the United States, 2011: The third FTC survey. Federal Trade Commission. April 2013. Accessed October 26, 2021. 

https://www.ftc.gov/sites/default/files/documents/reports/consumer-fraud-united-states-2011-third-ftc-survey/130419fraudsurvey_0.pdf

Elder abuse as a risk factor for hospitalization in older persons

Exploitation in older adults: social vulnerability and personal competence factors

Grey matter correlates of susceptibility to scams in community-dwelling older adults.

APS investigation across four types of elder maltreatment.

Poor decision making is a consequence of cognitive decline among older persons without Alzheimer’s disease or mild cognitive impairment

12. Hebert LE, Scherr PA, Bienias JL, et al. 

Alzheimer disease in the US population: prevalence estimates using the 2000 census

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14. Catalano LA, Lazaro C. Financial abuse of elderly investors: protecting the vulnerable

Journal of Securities Law, Regulation & Compliance

Correlates of susceptibility to scams in older adults without dementia

16. Boyle PA, Yu L, Schneider JA, et al. 

Scam awareness related to incident Alzheimer dementia and mild cognitive impairment: a prospective cohort study

17. Marson DC, Martin RC, Wadley V, et al. 

Clinical interview assessment of financial capacity in older adults with mild cognitive impairment and Alzheimer's disease

18. Earnst KS, Wadley VG, Aldridge TM, et al. 

Loss of financial capacity in Alzheimer's disease: the role of working memory.

Theoretical frameworks for competency in cognitively impaired elderly adults

The Journey of Caregiving: Honor, Responsibility and Financial Complexity.

 Merrill Bank. 2017. Accessed October 26, 2021. 

https://images.em.bankofamerica.com/HOST-03-19-0704/AgeWaveCaregivingWhitepaper.pdf

With the growing elderly population and the prevalence of cognitive impairment, how can we protect older adults from financial scams?

Vulnerability to Financial Scamming: Victim and Family Protection

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Although cognitive difficulties may not be the primary symptom addressed in patients with schizophrenia, these impairments are a 

 that can contribute to social and functional disability.

 Cognitive dysfunction in schizophrenia affects not only attention, verbal memory, reasoning, and processing speed, but also social 

 Thus, the topic has received increased attention. (For more information, see the 

A growing body of research results indicates viruses may play a role in both schizophrenia and cognitive difficulties. One in particular, Epstein-Barr virus (EBV), has received notable attention in the possible pathophysiology of schizophrenia as well as of associated cognitive dysfunction, although findings have been inconsistent. For instance, in 

y of 229 patients with schizophrenia, the data did not indicate an association between EBV seropositivity and cognitive performance.

 Importantly, previous studies have generally measured exposure by reactivity to a single EBV protein, rather than to a panel of proteins or EBV virions. EBV, also known as human herpesvirus 4, is a lymphotropic virus that can produce acute and latent infections.

Using the MATRICS Consensus Cognitive Battery (MCCB), 

 tested their hypothesis that antibodies to various EBV proteins may be associated with different levels and domains of cognitive functioning in patients with 

 Patients with schizophrenia or schizoaffective disorder were enrolled at the Stanley Research Program at Sheppard Pratt in Baltimore, Maryland, in 1 of 3 trials of adjunctive medications for adults with schizophrenia that were conducted between 2014 and 2019.

Across the 3 trials, inclusion criteria were: receiving outpatient (vs inpatient) treatment; aged > 18 years; diagnosis of schizophrenia/schizoaffective disorder confirmed by structured clinical interview; and current stable antipsychotic treatment. Patients were excluded from the study if they had clinically significant or unstable medical disorders; were pregnant or breastfeeding; had current or recent substance use disorder; or were found to have an intellectual disability or IQ below 70 (

 In addition to the MCCB, the psychopathology of each patient was assessed using the Positive and Negative Syndrome Scale (PANSS). The total sample size was 84 (

Blood was assayed for immunoglobulin G antibodies to EBV antigens derived from intact virions using enzyme immunoassay. Assay values for patients were compared with a standard score based on the reactivity of controls without psychiatric disorders. Reactivity to herpes simplex virus type 1 (HSV-1) was also measured by immunoassay. In all studies, blood samples and cognitive testing were completed before the administration of any study medication. Linear regression models were used to determine whether EBV antibodies (to the whole virion and to specific proteins) were associated with MCCB composite and domain scores (

), controlling for age, sex, race, education, smoking, and HSV-1 serology.

The authors found a significant association between the lower MCCB overall percentile composite score (ie, worse cognition) and higher levels of antibodies to the whole EBV virion, to the EBV nuclear antigen-1 (EBNA-1), and to the EBV viral capsid antigen (VCA). There was also a significant association between lower MCCB social cognition and higher level of EBV virion, EBNA-1, and VCA antibodies. Lower MCCB processing speed was associated with higher EBV virion antibodies at a trend level. Lower MCCB working memory was also associated with higher EBNA-1 antibodies at a trend level.

The authors concluded that worse cognitive functioning in schizophrenia was associated with specific patterns of reactivity to EBV, including global and social cognition. Dickerson and colleagues acknowledged both strengths and limitations of their study. For instance, the present study includes the comprehensive cognitive battery (MCCB) and the measurement of EBV reactivity to specific EBV proteins. The investigators noted that the biological basis for the association between cognitive functioning and immune response to EBV is unknown. However, this study included a relatively small sample size, so the results may not be generalizable to other samples of patients with schizophrenia. Similarly, there may be possible residual confounding effects (eg, diet, genetics).

Exposure to EBV may contribute to cognitive impairments in patients with schizophrenia, which may have clinical implications. In particular, certain antiviral medications may be relevant to the prevention and treatment of EBV-associated cognitive impairment.

Regardless of these findings, it is important for clinicians to remain vigilant in the identification and assessment of cognitive impairment in schizophrenia, given its impact on social and functional disability. Although there are not any approved medications, clinicians can potentially improve cognitive outcomes by optimizing antipsychotic dosing based on symptoms and adverse effects, treating underlying depression, facilitating treatment of medical comorbidities (eg, hypertension, diabetes), and utilizing other therapies (eg, cognitive remediation) as available and appropriate.

is a professor in the Department of Psychiatry and Health Behavior of Augusta University in Augusta, Georgia. He is on the Editorial Board and serves as the schizophrenia section chief for 

The author reports that he receives research support from Augusta University, the National Institute of Mental Health, the Brain and Behavior Research Foundation, and the Stanley Medical Research Institute.

1. Dickerson F, Boronow JJ, Ringel N, Parente F. 

Neurocognitive deficits and social functioning in outpatients with schizophrenia

3. Dickerson FB, Boronow JJ, Stallings C, et al. 

Association of serum antibodies to herpes simplex virus 1 with cognitive deficits in individuals with schizophrenia

. Arch Gen Psychiatry. 2003;60(5):466-472.

4. Dickerson F, Katsafanas E, Origoni A, et al. 

Exposure to Epstein Barr virus and cognitive functioning in individuals with schizophrenia

5. MCCB [MATRICS Consensus Cognitive Battery] Neuropsychological Assessment. MATRICS Assessment Inc. Accessed February 4, 2021. 

A growing body of scientific literature makes the case.

Is Epstein-Barr Virus to Blame for Cognition in Schizophrenia?

The world is in the midst of an unfolding cognition crisis, with devastating personal, societal, and economic implications. The expanding elderly population requires better cognitive care; we are also coming to understand the importance of cognitive interventions and support in early childhood. Furthermore, the COVID-19 pandemic has brought global attention to cognitive issues, with over 50% of individuals recovering from the infection experiencing fatigue and brain fog. Initial studies indicate lasting deficits in executive function, impaired cognitive control, and reduction in global cognition leading to disability or reduced function.

 There are fears that COVID-induced deficits may last for years beyond the infection.

—such as attention, memory, perception, language, and reasoning

—are declining across the whole population. Beyond the effects of COVID-19, there is an alarming increase in the number of individuals around the world with serious cognitive impairments. These impairments co-occur with disorders including depression, anxiety, schizophrenia, autism, posttraumatic stress disorder, dyslexia, obsessive-compulsive disorder, bipolar disorder, attention-deficit/hyperactivity disorder (ADHD), addiction, dementias, and more.

 The severity, type, duration, and course of cognitive dysfunction differ between these disorders. The aging world population will heighten the cognition crisis. By 2060, the 

number of individuals aged 65 and older is projected to double

 is often only assessed when there is a specific, subjective complaint from patients, family members, or caregivers. In this context, there are many factors which suboptimize the value. For example, there are lengthy waiting lists to see neuropsychologists or cognitive neurologists, and various modalities used to assess cognitive dysfunction in later life are inaccessible to most (eg, positron emission tomography and advanced magnetic resonance imaging scans). Furthermore, there is no consistent clinical assessment algorithm for how to use cognitive assessment tools (eg, when to use pencil and paper tests, digital, blood-based, or neuroimaging). When there is no specific, subjective cognitive complaint, cognition is not assessed. This means more subtle and slow-onset forms of cognitive dysfunction may be missed. This can delay treatment and mean more progressive brain changes. If cognition is assessed, it is often not addressed, supported, or followed up in the long-term. Further, in many developing countries, cognition is rarely—if ever—screened, resulting in complications such as high rates of undiagnosed dementia.

 across the lifespan, it is critical that cognition is assessed and monitored across disorders and throughout life. Addressing and building cognition is especially crucial during early childhood, when cognitive difficulties can be caught before they have too much detrimental impact on a child’s developmental trajectory.

Examples of Cognitive Decline in Psychiatric Conditions

Consider depression: More than 264 million individuals around the world suffer from depression, making it the 

 and a major contributor to the overall global burden of disease.

 Depression is commonly associated with a lowering of a patient’s mood and energy for long periods of time. Depression also impairs cognition, including affecting attention, memory, information processing, decision-making skills, cognitive flexibility, and executive functioning.

 Indeed, 85 to 94% of individuals with acute depression experience significant cognitive impairments.

The world is facing a cognition crisis. Here’s how to face it with measurement-based cognitive care.

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