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Program

19th ANNUAL MILD COGNITIVE IMPAIRMENT SYMPOSIUM
Saturday, February 27, 2021 (10:00 am – 4:30 pm US Eastern Time)
Sunday, February 28, 2021 (10:00 am – 1:15 pm US Eastern Time)

SPECIAL TOPIC WORKSHOP
Sunday, February 28, 2021 (1:30 pm – 5:00 pm US Eastern Time)

THE ANNUAL ALZHEIMER’S PUBLIC EDUCATIONAL FORUM
Sunday, March 7, 2021 (1:30 pm – 3:30 pm US Eastern Time)

If you have registered on or before the 27th of February, 8pm US Eastern Time:

  • you should have received an email with instructions to access the virtual hub of the meeting. Please check your spam folder as well.
  • you can access the Symposium’s virtual hub (the first time), by clicking on “reset password” at that page and following the instructions received in the email. Please check your spam box, once more.

If you register after the above date and time, please note that access information will be provided with some delay though we will do our best to support all “at-door” registrations.

PLEASE NOTE THAT THE PUBLIC EDUCATIONAL FORUM IS SCHEDULED FOR SUNDAY, MARCH 7, 1:30 PM US EASTERN TIME.

Schedule

MCI Symposium Program (Day 1)

Saturday, February 27, 2021

All times in US Eastern Time.

10:00 am
Welcome Remarks
10:10
Symposium Introductory Notes
10:20
SESSION 1: Utility of Blood Biomarkers in the Diagnosis of Pre-Clinical and Clinical AD - Chair: Henrik Zetterberg, MD, PhD, University of Gothenburg
10:20
Session Overview
10:25
KEYNOTE LECTURE: Recent Developments in the Clinical Application of Blood Biomarkers for Screening and Diagnosis of AD and other Neurodegenerative Diseases
11:00
Utility of Blood Biomarkers for AD Diagnosis – Experience from the SEABIRD Study
11:20
Utility of Blood Biomarkers for AD Diagnosis – Experience from the BioFinder Study
11:40
Utility of Blood Biomarkers for AD Diagnosis – Experience from the Rotterdam Study
12:00 pm
Utility of Blood Biomarkers for Distinguishing between AD and FTLD
12:20
Panel Discussion/Q&A
12:45
SHORT PRESENTATIONS
1:15
Break
1:30
SESSION 2: Sensory Disorders (Olfaction Hearing and Visual Deficits) in Preclinical AD and Early MCI - Chair: Shannon Risacher, PhD, Indiana University
1:30
Session Overview
1:35
KEYNOTE LECTURE: Multidomain Sensory Measures as Biomarkers of Preclinical and Prodromal AD
2:00
Association of Visual Acuity to Cognitive Impairment and Cognitive Decline
2:20
Deficit in Central Auditory Processing as a Biomarker of Pre-Clinical Alzheimer’s Disease
2:40
Association of Olfactory Identification Deficits with Amyloid, Tau and Inflammatory Pathology in the Brain
3:00
Delivering Novel Neuro Retinal Biomarkers for Early Diagnosis of Alzheimer's Disease
3:20
Age-related Sensory Deficits and Their Consequences
3:40
Panel Discussion/Q&A
4:00
SHORT PRESENTATIONS
4:30
END OF DAY 1
10:00 am
Ranjan Duara, MD, FAAN - Mount Sinai Medical Center
10:10
Ronald Petersen, MD, PhD - Mayo Clinic
10:20
Chair: Henrik Zetterberg, MD, PhD, University of Gothenburg
10:20
Henrik Zetterberg, MD, PhD - University of Gothenburg
10:25
Henrik Zetterberg, MD, PhD - University of Gothenburg
11:00
Suzanne Schindler, MD, PhD - Washington University School of Medicine
11:20
Oskar Hansson, MD, PhD - Lund University
11:40
Mohammad Arfan Ikram, MD, PhD - Erasmus University Medical Center
12:00 pm
Elisabeth Thijssen, MSc - University of California, San Francisco/Amsterdam UMC
12:20
Panel Discussion/Q&A
12:45
SHORT PRESENTATIONS
1:15
Break
1:30
Chair: Shannon Risacher, PhD - Indiana University
1:30
Shannon Risacher, PhD - Indiana University
1:35
Shannon Risacher, PhD - Indiana University
2:00
Beth Snitz, PhD - University of Pittsburgh
2:20
John Breitner, MD - McGill University
2:40
William C. Kreisl, MD - Columbia University
3:00
Peter Van Wijngaarden, MD - Centre for Eye Research Australia
3:20
Willa Brenowitz, PhD, MPH - University of California, San Francisco
3:40
Panel Discussion/Q&A
4:00
SHORT PRESENTATIONS
4:30
END OF DAY 1

MCI Symposium Program (Day 2)

Sunday, February 28, 2021

All times in US Eastern Time.

10:00 am
SESSION 3: Vascular MCI
10:00
Session Overview
10:05
KEYNOTE LECTURE: Neurovascular Coupling in Health and Disease - The Grey Zone between Vascular Cognitive Impairment and MCI-AD
10:40
Vascular Mild Cognitive Impairment
11:00
Vascular Cognitive Impairment Associated with Subcortical Small-Vessel Disease
11:20
Relevance of Brain Lesion Location for Cognition in Vascular Mild Cognitive Impairment
11:40
The Complex Profiles of Cerebrovascular Disease Pathologies in the Aging Brain and Their Relationship with Cognitive Decline
12:00 pm
Association of Perivascular Space Enlargement and Cognitive Impairment
12:20
Panel Discussion/Q&A
12:45
SHORT PRESENTATIONS
1:15
END OF SYMPOSIUM
10:00 am
Sandra Black, MD - Sunnybrook Research Institute
10:00
Sandra Black, MD - Sunnybrook Research Institute
10:05
Costantino Iadecola, MD - Weill Cornell Medicine
10:40
Sandra Black, MD - Sunnybrook Research Institute
11:00
Helena Chang Chui, MD - University of Southern California
11:20
Oscar Lopez, MD - University of Pittsburgh
11:40
Melissa Lamar, PhD - Rush University
12:00 pm
Tatjana Rundek, MD, PhD - University of Miami, Miller School of Medicine
12:20
Panel Discussion/Q&A
12:45
SHORT PRESENTATIONS
1:15
END OF SYMPOSIUM

Special Topic Workshop Program

Sunday, February 28, 2021

All times in US Eastern Time.

1:30 pm
Introductory Notes
1:35
KEYNOTE LECTURE: Locus of Control and Cognitive Performance in Adulthood

Locus of Control (LoC) is the degree to which people believe that they, as opposed to external forces, have control over the outcome of events in their lives. An ‘external’ LoC supports a belief that one is not in control of life events (e.g. successes and failures); an ‘internal’ LoC supports the belief that life events are due to one’s own efforts. LoC has been adversely associated with many psychological and physical health outcomes over the previous two decades, with a general view that greater externality is associated with poorer health outcomes such as obesity and depression. However, few studies have examined whether it is related to cognitive function in adulthood. Given treatments for cognitive decline are sparse and very few modifiable risk factors have been identified to inform prevention strategies, we examined the effect of LoC on cognitive function in adulthood.

In 1178 women from the Avon Longitudinal Study of Parents And Children, we examined the association between LoC, and change in LoC over almost 20 years, with cognitive function in midlife. LoC was prospectively measured at mean ages 30 and 48 years, using the widely validated Nowicki-Strickland scale. Cognitive function was examined at mean age 51 years.

Greater externality was consistently associated with lower cognitive function. For example, women classified as being external at mean age 48 years had, on average, a 0.18 lower cognitive function score (95% CI: 0.11 to 0.25) than the group classified as being internal (p<0.001). Participants who changed from external to internal over time, on average, had better cognitive function than those who remained external or changed to become external.

In summary, an external LoC is likely to be detrimental to cognitive function. Interventions to increase internality may help to minimise the adverse consequences on cognitive health later in life. Further studies should try to elucidate the mechanisms through which externality may be detrimental to cognitive performance to highlight additional potential interventions.

2:10
Cognitive and Neuroimaging Evidence for ADHD as a Phenotypic Mimic of Prodromal Dementia

Older adults seeking assessment for forgetfulness, absent-mindedness, and difficulty completing complex tasks, are usually worried they are exhibiting early signs of dementia. Careful documentation of symptom history, however, indicates that some represent undetected attention-deficit/hyperactivity disorder (ADHD), which may only manifest fully in later life (e.g., following changes to previously effective internal or external structures) and thus mimic a late-onset neurodegenerative syndrome. On the other hand, emerging research suggests ADHD may actually increase dementia risk. Two studies were undertaken to elucidate whether ADHD is more likely to be a phenotypic mimic (vs. a prodrome) of neurodegeneration.

A first study aimed to quantify the overlapping and unique features of ADHD and mild cognitive impairment (MCI, presumed to be a true dementia prodrome). Forty older adults with ADHD, 29 with MCI and 37 controls underwent neuropsychological assessment. A subsample (n=80) also underwent structural neuroimaging. Analyses revealed memory impairments in both patient groups, which reflected a storage deficit in MCI (supported by reduced hippocampal volumes) and an encoding deficit in ADHD (supported by frontal-lobe cortical thinning). Semantic retrieval was uniquely impaired in MCI.

A second study constituted a retrospective chart review of six older adults with ADHD with repeated clinical neuropsychological assessment across 5 to 21 years. Longitudinal performance was inspected to determine the extent of cognitive change. Overall, most participants performed normally on measures of attention, language, speeded switching and working memory. Four participants had at least one time point at which memory was impaired, but no participants’ abilities declined notably across time. Visuo-constructional abilities and cognitive flexibility were borderline to impaired in most participants across all time points but showed no significant decline. There were no obvious relationships between fluctuations in cognitive performance and depressive symptoms.

In conclusion, both ADHD and MCI show important dementia-like features (i.e., memory deficits), which may cause ADHD to present as a pseudodementia syndrome. Overall different cognitive profiles (i.e., unique language and memory processes deficits in MCI) and neuroimaging profiles (i.e., frontal-lobe thinning in ADHD), along with generally stable cognition longitudinally in ADHD, tentatively suggest that it is not associated with neurodegeneration but rather mimicking its phenotypical presentation in some respects.

2:30
Stressful Events and Racial Disparities in Cognition

BACKGROUND: It is well-documented that African Americans are at elevated risk for cognitive impairment and dementia in late life, but reasons for the racial disparity remain underexplained. Stress processes have been linked to premature age-related morbidity, including cognitive impairment and risk for Alzheimer’s disease and related dementias (ADRD). Disproportionately high exposure to stressors among minoritized populations plausibly contributes to social disparities in cognitive aging.

OBJECTIVE: We examined the relationship between stressful life events and cognitive decline among African American and White participants enrolled in the Wisconsin Registry for Alzheimer’s Prevention (WRAP). METHODS: Linear mixed models including demographic, literacy, and health-related covariates were used to estimate (1) relationships between a life event index score and decline in cognitive test performance in two domains of executive function (Speed & Flexibility, Working Memory) and one domain of episodic memory (Verbal Learning & Memory) among 1,241 WRAP enrollees, stratified by race, and (2) contributions of stressful life events to racial differences in cognition within the full sample.

RESULTS: African Americans (N=50) reported more stressful life events than Whites (N=1,191). Higher stress scores associated with poorer Speed & Flexibility performance in both groups, though not with declines across time, and partially explained racial differentials in this domain. Among African Americans only, stressor exposure also associated with age-related decline in Verbal Learning & Memory. Stressor-cognition relationships were robust to adjustment for literacy and health-related variables.

CONCLUSIONS: Our findings are congruent with literature demonstrating that conditions of structural and interpersonal racism associate with stress exposure across the life course. In this study, greater lifetime stress predicted poorer later-life cognition, and, in a small sample of African Americans, faster declines in a key domain of episodic memory. This preliminary work suggests that future work in large minority aging cohorts should explore stress as an important source of modifiable, socially-rooted risk for impairment and ADRD in African Americans.

2:50
Break
3:00
Relationship between Cognitive Performance and Measures of Neurodegeneration among Hispanic and White Non-Hispanic Individuals

With an older population on the rise, and a greater ethnic representation among older adults in the U.S., investigations looking at AD pathogenesis focusing on the Hispanic population can offer new insights into the disease. The Hispanic ethnic minority is the fastest growing ethnic group and largest minority group in the U.S. and they are nearly 1.5 times more likely to develop AD and other dementia diagnoses than White non-Hispanic (WNH) individuals. The aim of this special topic workshop is to review results of studies conducted by the 1FLADRC where cultural factors are examined in relation to cognitive decline and AD pathology.

One study identified that acculturation level and literacy contribute to performance on traditional neuropsychological tests among Hispanic older adults. Specifically, we found that acculturation level may hinder performance on verbal learning measures and high literacy is associated with better performance on language measures, but with more brain atrophy in AD prone regions. In another study, we examined neurodegeneration (as measured by MRI) among Hispanic and WNH participants with equivalent levels of clinical function, as measured by a culture fair cognitive test and the CDR. We found that despite equivalent levels of performance on these measures, there was a difference in levels of neurodegeneration in medial temporal areas, with WNHs showing more brain atrophy. The results of these and other studies will be discussed.

In conclusion, our results are consistent with existing literature and indicate that poor performance on cognitive testing may not accurately represent AD pathology among Hispanic older adults. Additionally, there is evidence to suggest different rates of neurodegeneration between Hispanic and WNH which can be influenced by factors such as acculturation level, literacy, education, and biological sex.

3:20
Cognitive Assessment and Mild Cognitive Impairment among Diverse Latinos

Mild cognitive impairment is defined by cognitive impairment and decline along with subjective and/or informant-based cognitive complaints. Objectively, defining these MCI cognitive traits among Latinos in general brings inherent challenges and complexities, which are manifold when assessing Latinos of diverse backgrounds. The purpose of this seminar is to describe the inherent challenges to MCI cognitive assessment of diverse Latinos and approaches for overcoming some these challenges. Experiences and findings used in the Study of Latinos-Investigation of Neurocognitive Aging (SOL-INCA) will be used to illustrate some of the challenges and approaches for defining cognitive impairment and decline amongst diverse Latinos in the US. Data access and forthcoming cognitive assessment resources for practitioners and researchers investigating cognitive function and MCI among diverse Latinos will be described and shared with attendees of this Special Topic Workshop.

3:40
Pseudodementia, Pseudopseudodementia and Pseudodepression

While most older people who develop problems with their memory and thinking that are severe enough to impair their ability to function in everyday life typically, are found to have Alzheimer’s disease or other neurodegenerative diseases, some have an undiagnosed and treatable psychiatric disorder masquerading as dementia. These conditions including depression can affect memory and thinking and, when severe, create a clinical picture similar to dementia. This phenomenon, known as “pseudodementia”, is encountered in clinical practice. It is important to identify because it may be reversible with appropriate treatment.

There is controversy about what the longer-term prognosis is for people diagnosed with pseudodementia. This has implications for how to manage patients, what advice to give to patients and their family, and how to conceptualise the disorder. Some studies found that people with pseudodementia eventually develop organic dementia, so called pseudo-pseudodementia. To address this, we conducted a systematic review of studies that had been conducted on pseudodementia and which followed up patients over time.

Eighteen studies followed patients from several weeks to 18 years. Overall, patients with pseudodementia were at greater risk of later developing organic dementia. Importantly, not all patients did; many patients remained stable or improved, albeit some still impaired by their psychiatric disorder. Our review showed possible treatment benefits and differences with age; patients diagnosed with pseudodementia at a younger age had better outcomes. Finally, people with apathy (which is the commonest behavioural symptom in dementia) can be misdiagnosed as having depression, so called pseudo-depression and then often treated for the wrong condition. Patients with apathy do not respond to antidepressants.

Receiving the correct clinical diagnoses are crucial to patients receiving the correct treatment for their condition. A missed diagnosis of a potentially reversible depressive pseudodementia can have tragic consequence for the patient and family.

Recent research has neglected the study of pseudodementia. Our findings reveal a clear need for better diagnostic skills, further research with modern investigative tools, such as neuroimaging and genetic sequencing, and clinical trials to better understand underlying mechanisms and determine effective treatment strategies.

4:00
Panel Discussion/Q&A
4:25
Concluding Remarks
4:30
SHORT PRESENTATIONS
5:00
END OF WORKSHOP
1:30 pm
Mary Ganguli, MD, MPH - University of Pittsburgh
1:35
Emma Anderson, PhD - Bristol University

Locus of Control (LoC) is the degree to which people believe that they, as opposed to external forces, have control over the outcome of events in their lives. An ‘external’ LoC supports a belief that one is not in control of life events (e.g. successes and failures); an ‘internal’ LoC supports the belief that life events are due to one’s own efforts. LoC has been adversely associated with many psychological and physical health outcomes over the previous two decades, with a general view that greater externality is associated with poorer health outcomes such as obesity and depression. However, few studies have examined whether it is related to cognitive function in adulthood. Given treatments for cognitive decline are sparse and very few modifiable risk factors have been identified to inform prevention strategies, we examined the effect of LoC on cognitive function in adulthood.

In 1178 women from the Avon Longitudinal Study of Parents And Children, we examined the association between LoC, and change in LoC over almost 20 years, with cognitive function in midlife. LoC was prospectively measured at mean ages 30 and 48 years, using the widely validated Nowicki-Strickland scale. Cognitive function was examined at mean age 51 years.

Greater externality was consistently associated with lower cognitive function. For example, women classified as being external at mean age 48 years had, on average, a 0.18 lower cognitive function score (95% CI: 0.11 to 0.25) than the group classified as being internal (p<0.001). Participants who changed from external to internal over time, on average, had better cognitive function than those who remained external or changed to become external.

In summary, an external LoC is likely to be detrimental to cognitive function. Interventions to increase internality may help to minimise the adverse consequences on cognitive health later in life. Further studies should try to elucidate the mechanisms through which externality may be detrimental to cognitive performance to highlight additional potential interventions.

2:10
Brandy Callahan, PhD - University of Calgary

Older adults seeking assessment for forgetfulness, absent-mindedness, and difficulty completing complex tasks, are usually worried they are exhibiting early signs of dementia. Careful documentation of symptom history, however, indicates that some represent undetected attention-deficit/hyperactivity disorder (ADHD), which may only manifest fully in later life (e.g., following changes to previously effective internal or external structures) and thus mimic a late-onset neurodegenerative syndrome. On the other hand, emerging research suggests ADHD may actually increase dementia risk. Two studies were undertaken to elucidate whether ADHD is more likely to be a phenotypic mimic (vs. a prodrome) of neurodegeneration.

A first study aimed to quantify the overlapping and unique features of ADHD and mild cognitive impairment (MCI, presumed to be a true dementia prodrome). Forty older adults with ADHD, 29 with MCI and 37 controls underwent neuropsychological assessment. A subsample (n=80) also underwent structural neuroimaging. Analyses revealed memory impairments in both patient groups, which reflected a storage deficit in MCI (supported by reduced hippocampal volumes) and an encoding deficit in ADHD (supported by frontal-lobe cortical thinning). Semantic retrieval was uniquely impaired in MCI.

A second study constituted a retrospective chart review of six older adults with ADHD with repeated clinical neuropsychological assessment across 5 to 21 years. Longitudinal performance was inspected to determine the extent of cognitive change. Overall, most participants performed normally on measures of attention, language, speeded switching and working memory. Four participants had at least one time point at which memory was impaired, but no participants’ abilities declined notably across time. Visuo-constructional abilities and cognitive flexibility were borderline to impaired in most participants across all time points but showed no significant decline. There were no obvious relationships between fluctuations in cognitive performance and depressive symptoms.

In conclusion, both ADHD and MCI show important dementia-like features (i.e., memory deficits), which may cause ADHD to present as a pseudodementia syndrome. Overall different cognitive profiles (i.e., unique language and memory processes deficits in MCI) and neuroimaging profiles (i.e., frontal-lobe thinning in ADHD), along with generally stable cognition longitudinally in ADHD, tentatively suggest that it is not associated with neurodegeneration but rather mimicking its phenotypical presentation in some respects.

2:30
Megan Zuelsdorff, PhD - University of Wisconsin, Madison

BACKGROUND: It is well-documented that African Americans are at elevated risk for cognitive impairment and dementia in late life, but reasons for the racial disparity remain underexplained. Stress processes have been linked to premature age-related morbidity, including cognitive impairment and risk for Alzheimer’s disease and related dementias (ADRD). Disproportionately high exposure to stressors among minoritized populations plausibly contributes to social disparities in cognitive aging.

OBJECTIVE: We examined the relationship between stressful life events and cognitive decline among African American and White participants enrolled in the Wisconsin Registry for Alzheimer’s Prevention (WRAP). METHODS: Linear mixed models including demographic, literacy, and health-related covariates were used to estimate (1) relationships between a life event index score and decline in cognitive test performance in two domains of executive function (Speed & Flexibility, Working Memory) and one domain of episodic memory (Verbal Learning & Memory) among 1,241 WRAP enrollees, stratified by race, and (2) contributions of stressful life events to racial differences in cognition within the full sample.

RESULTS: African Americans (N=50) reported more stressful life events than Whites (N=1,191). Higher stress scores associated with poorer Speed & Flexibility performance in both groups, though not with declines across time, and partially explained racial differentials in this domain. Among African Americans only, stressor exposure also associated with age-related decline in Verbal Learning & Memory. Stressor-cognition relationships were robust to adjustment for literacy and health-related variables.

CONCLUSIONS: Our findings are congruent with literature demonstrating that conditions of structural and interpersonal racism associate with stress exposure across the life course. In this study, greater lifetime stress predicted poorer later-life cognition, and, in a small sample of African Americans, faster declines in a key domain of episodic memory. This preliminary work suggests that future work in large minority aging cohorts should explore stress as an important source of modifiable, socially-rooted risk for impairment and ADRD in African Americans.

2:50
Break
3:00
Miriam Rodriguez, PhD - Albizu University

With an older population on the rise, and a greater ethnic representation among older adults in the U.S., investigations looking at AD pathogenesis focusing on the Hispanic population can offer new insights into the disease. The Hispanic ethnic minority is the fastest growing ethnic group and largest minority group in the U.S. and they are nearly 1.5 times more likely to develop AD and other dementia diagnoses than White non-Hispanic (WNH) individuals. The aim of this special topic workshop is to review results of studies conducted by the 1FLADRC where cultural factors are examined in relation to cognitive decline and AD pathology.

One study identified that acculturation level and literacy contribute to performance on traditional neuropsychological tests among Hispanic older adults. Specifically, we found that acculturation level may hinder performance on verbal learning measures and high literacy is associated with better performance on language measures, but with more brain atrophy in AD prone regions. In another study, we examined neurodegeneration (as measured by MRI) among Hispanic and WNH participants with equivalent levels of clinical function, as measured by a culture fair cognitive test and the CDR. We found that despite equivalent levels of performance on these measures, there was a difference in levels of neurodegeneration in medial temporal areas, with WNHs showing more brain atrophy. The results of these and other studies will be discussed.

In conclusion, our results are consistent with existing literature and indicate that poor performance on cognitive testing may not accurately represent AD pathology among Hispanic older adults. Additionally, there is evidence to suggest different rates of neurodegeneration between Hispanic and WNH which can be influenced by factors such as acculturation level, literacy, education, and biological sex.

3:20
Hector Gonzalez, PhD - University of California, San Diego

Mild cognitive impairment is defined by cognitive impairment and decline along with subjective and/or informant-based cognitive complaints. Objectively, defining these MCI cognitive traits among Latinos in general brings inherent challenges and complexities, which are manifold when assessing Latinos of diverse backgrounds. The purpose of this seminar is to describe the inherent challenges to MCI cognitive assessment of diverse Latinos and approaches for overcoming some these challenges. Experiences and findings used in the Study of Latinos-Investigation of Neurocognitive Aging (SOL-INCA) will be used to illustrate some of the challenges and approaches for defining cognitive impairment and decline amongst diverse Latinos in the US. Data access and forthcoming cognitive assessment resources for practitioners and researchers investigating cognitive function and MCI among diverse Latinos will be described and shared with attendees of this Special Topic Workshop.

3:40
Henry Brodaty, MD - University of New South Wales

While most older people who develop problems with their memory and thinking that are severe enough to impair their ability to function in everyday life typically, are found to have Alzheimer’s disease or other neurodegenerative diseases, some have an undiagnosed and treatable psychiatric disorder masquerading as dementia. These conditions including depression can affect memory and thinking and, when severe, create a clinical picture similar to dementia. This phenomenon, known as “pseudodementia”, is encountered in clinical practice. It is important to identify because it may be reversible with appropriate treatment.

There is controversy about what the longer-term prognosis is for people diagnosed with pseudodementia. This has implications for how to manage patients, what advice to give to patients and their family, and how to conceptualise the disorder. Some studies found that people with pseudodementia eventually develop organic dementia, so called pseudo-pseudodementia. To address this, we conducted a systematic review of studies that had been conducted on pseudodementia and which followed up patients over time.

Eighteen studies followed patients from several weeks to 18 years. Overall, patients with pseudodementia were at greater risk of later developing organic dementia. Importantly, not all patients did; many patients remained stable or improved, albeit some still impaired by their psychiatric disorder. Our review showed possible treatment benefits and differences with age; patients diagnosed with pseudodementia at a younger age had better outcomes. Finally, people with apathy (which is the commonest behavioural symptom in dementia) can be misdiagnosed as having depression, so called pseudo-depression and then often treated for the wrong condition. Patients with apathy do not respond to antidepressants.

Receiving the correct clinical diagnoses are crucial to patients receiving the correct treatment for their condition. A missed diagnosis of a potentially reversible depressive pseudodementia can have tragic consequence for the patient and family.

Recent research has neglected the study of pseudodementia. Our findings reveal a clear need for better diagnostic skills, further research with modern investigative tools, such as neuroimaging and genetic sequencing, and clinical trials to better understand underlying mechanisms and determine effective treatment strategies.

4:00
Panel Discussion/Q&A
4:25
Ranjan Duara, MD, FAAN - Mount Sinai Medical Center
4:30
SHORT PRESENTATIONS
5:00
END OF WORKSHOP

Public Educational Forum Program

Sunday, March 7, 2021

1:30 PM US Eastern Time.

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