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 covered a wide variety of psychiatric issues and industry updates, from evidence-based novel therapies for bipolar depression to potential indicators of early-stage Alzheimer disease. Here are some highlights from the week.

Thinking Beyond the Guidelines: Evidence-Based Novel Therapies for Bipolar Depression

Bipolar depression (BD) can be difficult to treat due to several factors, and choosing the most appropriate treatment approaches should be based upon patient-specific factors (eg, comorbidities, preferences). Based on treatment response and these patient-specific issues, there are a variety of nonpharmacologic therapies and novel pharmacologic options that can be considered as part of the treatment plan.

Although many clinicians tend to focus on pharmacologic treatments for BD, nonpharmacologic interventions have been shown to be effective in bipolar depression, many of which contribute to an overall healthy lifestyle and can be recommended in addition to medications. Additionally, some of these interventions pose only a low risk, and they may be preferable to the use of medications for select patients. Barriers associated with implementation include cost and accessibility. Clinicians should familiarize themselves with the following interventions and recommend them to patients whenever possible. 

Formic Acid as a Urinary Biomarker for Early-Stage Alzheimer Disease

A new study is the first to identify formic acid as a sensitive urinary biomarker that can reveal early-stage Alzheimer disease.Investigators found that urinary formic acid is a sensitive marker of subjective cognitive decline that may indicate the very early stages of Alzheimer disease. A noninvasive, inexpensive urine test for formic acid could help improve the rate of diagnosis, which often comes too late for effective treatment.

“Alzheimer disease is a continuous and concealed chronic disease, meaning that it can develop and last for many years before obvious cognitive impairment emerges,” said the authors. “The early stages of the disease occur before the irreversible dementia stage, and this is the golden window for intervention and treatment. Therefore, large-scale screening for early-stage Alzheimer disease is necessary for the elderly.” 

As I have been writing this daily blog this morning, the sun has been coming up, dispelling the darkness. “Gaslighting” had been brought to my attention by a colleague. On this past Tuesday, it was revealed as Merriam-Webster’s Word of the Year, based solely on the data on most-searched words, excluding the timeless ones. Two definitions were provided, a long and a short one:

“Psychological manipulation of a person usually over an extended period of time that causes the victim to question the validity of their own thoughts, perception of reality, or memories and typically leads to confusion, loss of confidence and self-esteem, uncertainty of one’s emotional or mental stability, and a dependency on the perpetrator.”

Or more succinctly, “the act or practice of grossly misleading someone especially for one’s own advantage.” 

Being well versed in correct terminology is fundamental to building affirming clinical environments and psychosocial rapport with patients. Physicians are not expected to get everything right, but to take responsibility for their education and apologize in the event a mistake is made.

 a key distinction to make is between sex and gender. Sex is assigned at birth by a medical professional most often based on biological criteria, such as external genitalia. Gender refers to a person’s internal sense of self, which can be expressed through a diverse range of social, cultural, physical, and behavioral cues, such as clothing, pronouns, and physical embodiment.

 neither sex nor gender are binary, as evidenced by the existence of intersex and TGD individuals. And neither sex nor gender are categorical. Someone’s gender identity can change through their life, and someone’s sex can, too (eg, a person can change their gender expression, sex hormone levels, and the appearance of their genitalia). 

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Do you have a comment on any of these or other articles? Have a good idea for an article and want to write? Interested in sharing your perspectives? Write to us at 

From evidence-based novel therapies for bipolar depression to potential indicators of early-stage Alzheimer disease, here are highlights from the week in Psychiatric Times.

The Week in Review: November 28-December 2

A study found that intranasal (IN) delivery of an oxytocin derivative to the brain may be an effective treatment for cognitive disorders such as Alzheimer disease.

Leveraging previous research suggesting that introducing cell-penetrating peptides (CPPs) and a penetration-accelerating sequence (PAS) via structural modifications can benefit the nose-to-brain delivery pathway, the investigators created the oxytocin derivative PAS-CPPs-oxytocin. Their goal was to see if IN delivery of this oxytocin derivative would help improve cognitive function in mice similarly to the more invasive intracerebroventricular (ICV) administration method.

“We have previously shown that oxytocin reverses amyloid 𝛽 peptide (25-35) (A𝛽

)-induced impairment of synaptic plasticity in rodents,” said corresponding author Jun-Ichiro Oka, PhD, in a press release. “We wanted to see if PAS-CPPs-oxytocin could be delivered more efficiently to the mouse brain for clinical application, and if it improved cognitive functional behavior in mice.”

The investigators conducted Y-maze and Morris water maze (MWM) tests and found that ICV delivery of oxytocin showed memory-improving effects on the Aβ

-induced amnesia in both the Y-maze and MWM tests, while IN administration of the oxytocin derivative showed memory-improving effects in the Y-maze test. The investigators also found evidence that, following its IN administration, the fluorescein isothiocyanate-labeled oxytocin derivative was distributed throughout the brain.

“My team is the first to show that the oxytocin derivative can improve the A𝛽

-induced memory impairment in mice,” Oka said in a press release. “This suggests that oxytocin may help reduce the cognitive decline we see in Alzheimer’s disease.”

Oka, who is on the faculty of pharmaceutical sciences at Tokyo University of Science, further clarified that these findings are clinically useful because “the oxytocin derivative enters the brain more efficiently. Furthermore, since IN delivery is a non-invasive procedure, this modified version of the hormone could potentially be a clinically viable treatment for Alzheimer’s disease.”

1. Takahashi J, Ueta Y, Yamada D, et al. 

Intracerebroventricular administration of oxytocin and intranasal administration of the oxytocin derivative improve β-amyloid peptide (25-23)-induced memory impairment in mice

2. Novel derivative of “love hormone” oxytocin improves cognition impairment in Alzheimer’s. Toyko University of Science. News release. October 24, 2022. Accessed November 4, 2022. 

https://www.tus.ac.jp/en/mediarelations/archive/20221021_1000.html

Results show comparisons between intranasal and intracerebroventricular distribution of an oxytocin derivative.

Study Identifies Promising Potential Treatment for Alzheimer Disease

Sadly, our retired sporting heroes often share more than memories, medals, and magical moments. Increasingly, many are united in suffering from chronic traumatic encephalopathy (CTE) as a result of repeated head injuries and concussions sustained during their competitive careers.

CTE is a condition that has been known for more than a century but is now recognized as prevalent among former stars of many high-impact sports including American football, soccer, rugby, boxing, and ice hockey. It shares features with Alzheimer disease (AD), but with possible research breakthroughs into treatment for AD, could we start to hope for a treatment for generations of sportspeople with the condition as well? 

Currently there are no disease-modifying therapies for the thousands of former sportspeople suffering from the memory loss, decline in cognitive abilities, confusion, depression, and behavioral changes that accompany the early-onset dementia stemming from CTE. Age of onset varies but it can be notably early in mid-life for many, resulting in a stark impact on quality of life. Cognitive impairment is often accompanied by physical symptoms that manifest as tremors and slurred speech.

In the United Kingdom, a group of 175 current and former rugby players, both male and female, are part of a group legal action against the sport’s governing bodies because they have been diagnosed with traumatic brain injury (TBI), early onset dementia, and CTE.

 Indeed, the 8 former professional players who brought the initial case are all under 45 years old. The professional players leading the court case have heart-breaking stories to tell. Steve Thompson, for instance, cannot even remember winning the rugby World Cup with England in 2003 and wishes he had never played the game.

The claimants are looking to some compelling precedents. A decade ago, the National Football League (NFL), the governing body for American football in the United States, came to a settlement of $765 million, with more than 4500 former players, after conceding that head trauma could have serious lasting consequences.

Harrison Martland, MD, first reported the association between repetitive head trauma and neurodegeneration in a ground-breaking paper published in 1928. He described a series of boxers who developed a parkinsonian syndrome and mental deterioration later in life and were known as being “punch drunk.”

 His findings were reinforced in a 1973 paper, “The aftermath of boxing,” which described the classical pathological appearances of so-called “dementia pugilistica” and differentiated it from other neurodegenerative diseases.

Omalu et al published the first case of CTE in a retired NFL player in 2005,

 and today, American football is the contact sport most commonly associated with autopsy proven CTE,

 with rates of more than 80% being reported in experienced players.

Among more recent compelling evidence, the FIELD study conducted at the University of Glasgow established that the risk of dementia among professional soccer players is almost 4 times higher than among their peers in the general population.

 Awareness of the issue was raised recently by media stories highlighting the prevalence of dementia among members of England’s 1966 World Cup-winning squad.

In response to demand, an international panel of experts called the Concussion in Sport Group (CISG) meets every 4 years to review the latest research and to set protocols on best practices for handling head injuries. So far, however, sports bodies have mainly focused on mitigating future risks such as moving to limit the amount of physical contact in training sessions (which account for as much as 90% of collisions experienced by professional rugby players) and to ban tackling for players under 18 years old. However, pitch-side management of athletes with minor head injuries across different sports remains inadequate in many instances.

Until now, there has not been much therapeutic research, and there have not been many clinical trials that could find potential solutions and offer peace of mind for those affected by CTE, or for the generations likely to be affected in the future. However, the disease process leading to CTE is now better understood due to the work of research teams studying pathological features in brains of former sportspeople.

CTE is a tauopathy but with a different pattern of tau pathology spread as compared to that seen in AD.

Researchers at TauRx have been studying tau pathology in AD for decades, focusing on the development of a tau aggregation inhibitor—currently in a late-stage clinical trial called Lucidity studying mild cognitive impairment due to AD and mild-moderate AD—in recognition of the established correlation between tau pathology and the rate of clinical decline in patients with AD.

CTE shares key features with AD. Tau protein in a healthy brain plays a critical role in microtubule stability, allowing for the effective transport of cell nutrients and neurotransmitters to the synapse. However, if the tau protein is caused to malfunction through brain injury (as in CTE) or age-related factors (as in AD), then it misfolds and causes other free tau protein to misfold and aggregate. This forms insoluble aggregated tau tangles and sets off a chain reaction of aggregation of abnormal tau. These tau aggregates can rapidly spread between cells leads to a point at which irreversible neuronal cell damage occurs.

Although CTE has been seen in young individuals, symptoms do not generally appear until years after the concussions or head impacts have been sustained, suggesting that there is a window of opportunity to intervene therapeutically.

Treatment of established CTE is currently limited to supportive measures with a variety of symptomatic medications currently used for AD and Parkinson disease, psychostimulants, and antidepressantsbut the evidence base is weak and there are currently no approved medications for CTE. However, greater understanding of tau pathology, as the common link between sports-related early-onset dementia and other tauopathies such as AD could offer a way forward. Clinical trial data suggests that tau aggregation inhibitors have potential to disassemble the tau tangles and allow the clearance of the tangled, or misfolded, proteins in order to slow clinical decline and reduce the damage to synaptic transmission and brain function.

Given that CTE is a tauopathy, research into tau-based therapeutics is the major focus for developing disease-modifying treatments. 

 including the related criteria for traumatic encephalopathy syndrome, or TES (

 are available and have been weighted toward the high specificity required for clinical trials.

Therapeutic research and clinical trials have the potential to find solutions and offer hope for those affected by CTE now, and for the generations likely to be affected in the future. Tau aggregation inhibition could prove to be a promising target for disease-modification in other non-AD tauopathies such as this.

A century after the identification of dementia pugilistica and punch-drunk syndrome, AD research may offer the key to effective treatment for the sporting heroes whose lives have been blighted by the sports to which they gave so much.

is a specialist anaesthetist, having worked as a consultant anaesthetist for 25 years. She entered pharmaceutical research when she began working as a sub investigator and principal investigator in London, focusing on Alzheimer disease. She joined TauRx in 2018 as medical oversight lead, responsible for patient safety in the TauRx trials. In her additional role as head of medical affairs, Dr Miller is responsible for relationships with external stakeholders and leads the information and education delivery resulting from TauRx’s research programs.

1. Pathak M. Rugby league former internationals to sue RFL over brain damage. Reuters. News release. October 27, 2021. Accessed September 1, 2022. 

https://www.reuters.com/world/uk/rugby-league-former-internationals-sue-rfl-over-brain-damage-2021-10-27/

2. Rugby World Cup winner Steve Thompson reveals he has dementia and joins landmark legal case. 

. December 8, 2020. Accessed September 1, 2022. 

https://www.theguardian.com/sport/2020/dec/08/steve-thompson-former-rugby-union-players-dementia-landmark-legal-case

3. Belson K. NFL agrees to settle concussion suit for $756 million. 

. August 29, 2013. Accessed September 1, 2022. 

https://www.nytimes.com/2013/08/30/sports/football/judge-announces-settlement-in-nfl-concussion-suit.html

5. Corsellis JA, Bruton CJ, Freeman-Browne D. 

6. Omalu BI, DeKosky ST, Minster RL, et al. 

Chronic traumatic encephalopathy in a National Football League player

7. Bieniek KF, Blessing MM, Heckman MG, et al. 

Association between contact sports participation and chronic traumatic encephalopathy: a retrospective cohort study

8. Mez J, Daneshvar DH, Kiernan PT, et al. 

Clinicopathological evaluation of chronic traumatic encephalopathy in players of American football

9. Smyth P. Consensus criteria for CTE clinical symptoms established. 

. March 22, 2021. Accessed September 1, 2022. 

https://www.physiciansweekly.com/consensus-criteria-for-cte-clinical-symptoms-established

10. Katz DI, Bernick C, Dodick DW, et al. 

National Institute of Neurological Disorders and Stroke consensus diagnostic criteria for traumatic encephalopathy syndrome

Can Alzheimer disease research offer the key to effective treatment? 

Treating Chronic Traumatic Encephalopathy in Athletes

On my most recent flight home (I know, I usually end up writing a new article every time I fly), I sat next to a middle-aged woman and her father who seems to be struggling with some kind of cognitive impairment, possibly 

. I was very impressed with how, throughout our 2.5-hour long flight, that she was quite attentive to his every need and kept him both engaged and entertained. She did that through asking questions and sharing pictures saved on her phone that seemed to fill his soul with joy.

Very few of us pay attention to our parents when they grow older, especially those with dementia. We seem to either take them for granted or get easily frustrated with them. Some of us even abandon them and then we wish for a different outcome when they are no longer with us.

I lost my mom in 2016. She was diagnosed with dementia during the ugly civil war in my home country, Libya. I do strongly believe that her memory quickly deteriorated because of the many times her heart broke losing loved ones to that nonsense. I was lucky to spend the last week of her life with her; I was holding her hand when she passed. She might have not remembered who I was, but I know deep in my heart that she felt I was there. I would have never had it any other way.

 before his death too. I remember him passing by my grandma’s room who died before him and him asking, “Where is the lady who used to be here?”

Maybe I am projecting my own fears about this ugly disease given that both my mom and her dad died of dementia-related complications. There is nothing I can do right now to change my genes or reduce my risk, but here are a few things I will do and encourage you to reflect on if one or both of your parent(s) is/are still alive:

1. Enjoy the current moment. Even if they do not have factual memories, create emotional memories for and with them, through moments of bonding, care, and tenderness.

2. Repair any damage in the relationship. Heal old wounds if there is room for healing. Forgive old ruptures if you can.

3. Focus on your spouse and children. Be emotionally available for them, so together you create long-lasting memories that they can cherish when they miss you.

4. Refuse the dysfunctional status quo. There is nothing normal about family breakdown.

5. Show respect, love, and compassion to the old people in your life and those around you. Not only your parents, but also your grandparents, uncles, aunts, older siblings and relatives, neighbors, and all seniors in your community. The global pandemic showed us how painful isolation is. The best cure for 

 is to build bridges and be a source of safety and solace for others.

6. And finally, do not forget to take care of yourself. Caregiving can bring joy, but can also lead to burnout if your neglect your own needs and boundaries.

Dementia is a mental health condition that can make or break families. Remember that behind the difficult behavior is your loved one—a human who deserves to be found, held, comforted, and tended to with the utmost love and compassion.

 is a practicing psychiatrist with Providence Healthcare System in Portland, Oregon. He is the author of 

The Wounded Healer: The Pain and Joy of Caregiving

A reminder to cherish your parents and the older adults in your life.

Dementia: A Social Death Sentence

 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

2. Boehmer TK, DeVies J, Caruso E, et al. 

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

3. Panagiotou OA, Kosar CM, White EM, et al. 

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

5. Levin AT, Hanage WP, Owusu-Boaitey N, et al. 

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

6. Tahira AC, Verjovski-Almeida S, Ferreira ST. 

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

10. Czeisler MÉ, Lane RI, Wiley JF, et al. 

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

20. García-Azorín D, Abildúa MJA, Aguirre MEE, et al; Spanish neuroCOVID registry group. 

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.

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

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