The meeting will address critical issues in psychopathology and aging from various perspectives – from the molecular to the societal level. There will be a focus on Alzheimer’s and other dementing illnesses as well as the outcomes of other types of mental disorders. Psychosocial and physical stressors common in later life (e.g., isolation, bereavement, failing health) increase risk of depression, demoralization, despair, and suicide. There will also be a focus on positive aspects of aging. The program includes prominent experts in various aging-related domains and the intended audience is researchers and clinicians interested in aging as well as students.
Anxiety in the elderly is associated with many challenges including decreased physical activity, decreased life satisfaction, and greater preoccupation with poor health compared to elderly individuals without clinical anxiety. Yet unlike geriatric depression, anxiety disorders in the elderly are relatively rarely studied despite the fact that the prevalence exceeds that of depression. In fact, these two conditions are highly comorbid in the elderly. Several barriers exist in screening and diagnosing anxiety in older adults including substantial medical comorbidity and increasing rates of cognitive impairment. Also, even at similar levels of severity some anxiety disorders present differently in the elderly compared to younger age groups. Some data exist on efficacious pharmacological and psychological treatments but certain medications such as benzodiazepines introduce complications. Also, limited information on treatment matching makes translation to practice difficult.
This talk first provides an overview of age dependent effects in attention deficit hyperactivity disorder (ADHD), including the age dependent decline in symptoms and the age dependent decline in volumetric brain changes associated with the disorder. While such data have been interpreted to indicate that ADHD associated volumetric brain changes disappear in adulthood, by applying a novel machine learning method, we show that the networks implicated in childhood ADHD are also implicated in adult ADHD. We also report new genomewide association data showing that child and adult ADHD share many common DNA variants in their polygenic source of etiology. We also present new data from the Swedish registries showing that ADHD predicts subsequent outcomes in later life of substantial public health significance. These include hypertension, type 2 diabetes, dementia and premature death.
The purpose of this lecture is to review the available literature on aging in Posttraumatic Stress Disorder (PTSD). There is a wealth of information in the mental health literature about the phenotypic components of PTSD in the elderly that compares and contrasts the symptomatology in PTSD in earlier developmental stages of adult life. There are fewer studies that follow the life course of people who were diagnosed with PTSD in an earlier developmental stage through to later stages. This talk will summarize the extant findings as they pertain to combat related PTSD in elderly patients. Further, information will be presented from Project VALOR, a longitudinal study initiated in 2008 with follow ups (four completed) continuing till the current time. Project VALOR is a national PTSD registry of 1649 veterans of the current wars; half are male and half female, and they are racially and ethnically representative of those using VA Healthcare. Seventy five percent of participants were selected to comprise the PTSD cohort while twenty-five percent are help seeking participants without PTSD or other Psychiatric conditions. Data for this Registry derive from the Electronic Medical Record, Diagnostic Interviews, and self report questionnaires. Findings across multiple domains of functioning will be presented characterizing the major issues affecting these military veterans over these past ten years.
The opioid epidemic among adolescents and adults across the US has been well documented, but the opioid and benzodiazepine prescription epidemic in the elderly has been largely ignored. Both opioids and benzodiazepines have profound physical, psychiatric and cognitive effects in older adults, however such medications continue to be prescribed in increasing numbers by physicians who are poorly trained in the insidious side effects of such medications and geriatrics as a whole. Unfortunately, ageism contributes to these prescriptions, as such medications are commonly used to treat psychiatric and behavioral disorders, with the general intent to sedate rather than treat the underlying disorder. In this presentation, rates and associated factors of benzodiazepine and opioid use in the elderly will be discussed in various settings including community and inpatient medical settings, as well as the psychiatric outpatient setting. Strategies for proper prescribing and appropriate treatments will be reviewed.
Emotional, behavioral and mental disorders are diagnosed in approximately 1/3 of all individuals diagnosed with Intellectual Disability/Intellectual Developmental Disorder (ID/IDD). The co-occurrence of these diagnoses contributes to their functional disability and is an additional burden for affected individuals and families already coping with the consequences of their cognitive and adaptive deficits. Those affected are burdened by continuing stigma; they remain in need of supports throughout their lives. With advances in medical care life expectancy is similar to that of the general population for those in the mild to moderate range of severity. It is estimated by the year 2030 there will be 1.2 million over age 60, a near doubling from the beginning of the 21st century. Aging adults with mild to moderate ID/IDD present with the full range of psychiatric symptoms and disorders similar to typically developing persons. Co-occurring mental disorders differ for those in the severe to profound range; especially impulse control disorders and self-injurious behavior. Dementia is more prevalent with aging in Down Syndrome and Psychosis in 22q11 deletion syndrome. With recognition of co-occurrence of disorders, the evidence base for effective personalized psychosocial, behavioral and pharmacotherapies is growing allowing affected individuals to be treated in community settings.
While there is no clear-cut basis for a simple dualistic distinction between “mental” and “physical” phenomena, in examining relationships between them, such a distinction can be a helpful heuristic. It is not always feasible to draw causal inferences when physical and mental disorders co-occur. We took advantage of data on major depression and PTSD among members of the Vietnam Era Twin Study when they were age 43 on average, and physical disorders with onset after age 43 reported during the Vietnam Era Twin Study of Aging when they were age 68 on average. We had polygenic risk scores available for a number of the disorders, allowing us to control for genetic vulnerability to the medical outcomes. Symptoms of depression and PTSD were each associated with incident diabetes and incident erectile dysfunction. Symptoms of depression, but not PTSD were associated with incident heart attack. Neither depression nor PTSD were associated with risk of stroke. We examined the relationship of depression and PTSD at age 43 to results of a modified Charlson Comorbidity Index (a list of medical illnesses predictive of 10-year mortality) at age 68. Both depression and PTSD were associated with higher scores on the Charlson. Putative mechanism mediating the observed relationships between the mental disorders and the physical outcomes will be discussed.
Basic principles of geriatric psychopharmacology include obtaining accurate information about past psychiatric illness (& treatments), current medical condition, knowledge of EVERYTHING that the patient is taking, including OTC meds and alcohol. Antipsychotics are still the first choice for severe dementia/psychosis agitation, but low doses of second generation drugs are preferred. Depressed elderly patients respond to antidepressants, but the mantra “start low, go slow” applies to these drugs, and all other psychotropic medications. Mood stabilizers also may require lower doses. Benzodiazepines may be helpful for anxiety and sleep but need to be used cautiously, at low doses and only short-half life drugs should be used used. Cholinesterase inhibitors (and memantine) are used to slow the progression of dementia, but do not reverse the disorder.
I will report on a prospective follow-up study of College men from age 18 to age 90 illustrating the determinants of aging physically, mentally and socially well. Relationships, smoking and alcohol history were very important; cholesterol and longevity of ancestors not very important.
The presentation will focus on recent research that has examined the effects of exercise training interventions and physical activity on cognitive and brain health. I will discuss research that has examined changes in brain structure and/or function along with behavioral measures of cognition in interventions lasting from several weeks to 1 year. Study populations will include children, young and middle-aged individuals, and the elderly in addition to a variety of patient groups. Although the focus will be on training to improve cardiorespiratory fitness I will also briefly cover resistance training and well as multi-modal cognitive and exercise training program. Finally, the presentation will identify gaps in the literature and potential solutions.
The pathological process in Alzheimer’s disease (AD) begins as much as 20 years before the onset of clinical dementia. Early identification is thus of paramount importance with respect to efforts to slow or prevent disease progression. Identifying mild cognitive impairment (MCI)—an early, pre-dementia stage of AD—is a step toward early identification, but the goal of early identification calls for going back even further to identify risk factors in cognitively normal adults for progression to MCI. The presentation contains a strong emphasis on neuropsychological function in both the diagnosis of MCI and the prediction of progression from normal cognitive function to MCI. I demonstrate how small improvements in the neuropsychological basis for defining cognitive impairment can make dramatic differences in diagnostic accuracy and prediction of progression to AD. I demonstrate that MCI can be diagnosed in middle age with extensive neuropsychological testing, and demonstrate its genetic risk. I also examine neuropsychological performance in cognitively normal individuals as a sensitive and very early predictor of risk for progression to MCI. I show that learning and practice effects can have significant effects on detection of MCI, and I examine neuropsychological features that may distinguish stable MCI cases from those that revert to normal cognition. Finally, rather than focusing on the ability of the hallmark AD biomarker, beta-amyloid, to predict disease progression, toward even earlier identification, I address the question of what predicts progression to amyloid positivity. Those results may call for modification of the AD continuum proposed as part of the recent A/T/(N) (amyloid/tau/neurodegeneration) research framework, and for the potential value of considering subthreshold biomarker levels.
Epidemiologic evidence indicates that lifestyle factors including educational and occupational attainment, engaging in leisure and social activities, as well as IQ are all associated with reduced risk of developing dementia. Many of these lifestyle factors have also been associated with reduced rate of cognitive decline in normal aging, and have a similar moderating influence on the expression and progression in many other brain diseases. The cognitive reserve hypothesis posits that individual differences in the flexibility and adaptability of brain networks underlying cognitive function may allow some people to cope better with age- or dementia-related brain changes than others. This is in contrast to the complementary concept of brain reserve, where the variability in the anatomic features of the brain itself provides reserve against pathology. Recent evidence also supports the idea that specific genetic and lifestyle factors may help preserve a healthy brain or enhance brain reserve, a process that has been called brain maintenance. This talk will review the development, epidemiologic and imaging support for these theoretical concepts, and current efforts intended to promote collaboration on reserve-related research including definitions, measure and research guidelines.
The National Institute on Aging (NIA) leads the Nation’s biomedical research enterprise on Alzheimer’s disease and related dementias (AD/ADRD). NIA’s research agenda for these areas of research has expanded since the release of the National Plan to Address Alzheimer’s disease in 2012 and subsequent significant appropriations from Congress. NIA supports broad, multidisciplinary AD/ADRD research programs in which research moves through a pipeline from studies of basic mechanisms to application in clinical trials, as well as research on care and caregiving. This presentation will review the diverse types of AD/ADRD research and programs that the NIA is supporting. Lastly, the presentation will outline some of the impacts of the recent investments on the AD/ADRD research field as a whole, including funding opportunities available to researchers.
There has been a call to action for treatments to prevent and effectively treat AD by 2025, with resulting development of national plans in many countries, well coordinated research efforts within multicountry research consortia and novel approaches including big data. In support of this effort the NIA budget for research in AD, has grown exponentially to over $ 2.3B annually. Despite these efforts, therapeutic progress has been disappointing. Over 200 experimental treatments have reached phase 2 development yet none have succeeded in phase 3.
This presentation, will review those therapeutic approaches that have been successful in reaching approval for symptomatic treatments, while addressing the unsuccessful approaches that have been undertaken in developing disease modifying treatments. Lessons learned and the dilemmas of amyloid lowering approaches will be addressed while characterizing the new directions within the current pipeline with emphasis on its need to diversify. The complexities of multiple targets, multiple pathologies, and need to personalize therapeutic approaches will also be addressed. The potential value of multidomain interventions to delay the onset or prevent AD, with emphasis on patient preferences, compliance and fidelity will be reviewed.
Depression predisposes to medical illnesses and advances biological aging indicated by shorter telomere length, accelerated brain aging and advanced epigenetic aging. Medical illnesses also increase the risk of late-life depression. The reciprocal relationships of depression with aging- and disease-related processes have generated pathogenetic hypotheses and provided treatment targets.
Targeting risk factors of vascular disease in mid-life is a logical approach to prevention of vascular depression. The depression-executive dysfunction and the vascular depression syndromes have clinical presentations and neuroimaging findings consistent with frontostriatal abnormalities. Dopamine D2/3 agonists are effective in depression of Parkinson’s disease and their efficacy needs to be assessed in these two syndromes. Modified Problem Solving Therapy has be found efficacious in the depression executive dysfunction syndrome of late-life. Computerized cognitive remediation targeting functions of the cognitive control network may improve both executive functions and depressive symptoms of late-life major depression. TMS targeting deep structures responsible for mood regulation is well tolerated by older adults and its efficacy in syndromes of late-life depression needs to be studied.
Efficacious psychotherapies for late-life depression exist but are underutilized in part because of their complexity. Streamlined, stepped psychotherapies targeting behaviors assumed to result from dysfunction of brain networks implicated in late-life depression can be easy to learn and have potential for dissemination. However, their effectiveness needs further investigation.
Suicide during later life poses particular challenges for prevention. Older adults take their own lives with high lethality of intent and utilize firearms more often than younger age groups. Suicide attempts are also less frequent and older adults less often express suicidal ideation than younger adults. While interventions must be aggressive in the actively suicidal older person, the lethality of suicidal behavior in older adults underscores the need for relatively greater emphasis on upstream preventive interventions.
In addition to access to deadly means, risk factors for completed suicide in later life can be characterized as “the 5 Ds”: demographic characteristics (male, older, unmarried), depression, disease (physical illness), disablement, and disconnectedness. Because older adults who take their own lives are more likely to be seen in primary care than mental health care settings, primary care-based integrated care models hold promise for reducing suicide in this age group. Social disconnectedness is also a modifiable state for which community-based services and supports should be mobilized.
At the conclusion of this talk, participants will understand the scope of the problem of suicide in older adults, factors that place older people at increased risk for suicide, and evidence for effective approaches to its prevention.
After first reviewing definitions and stages of bereavement, data on the mental and physical symptoms that randomly selected, recently bereaved experience in the first and thirteen month after the deaths of their spouses will be presented. Those symptoms will be compared to age and gender matched married community controls and psychiatric inpatients with major depression. Data on the experience of recent bereavement in psychiatric inpatients and matched hospital controls will also be presented. Finally, good and bad outcomes for the recently bereaved will be presented.
With the meeting’s them of “psychopathology and aging,” it is fitting that my talk, scheduled at the end of the program, addresses mental health at the end-of-life. As we age, we inevitably confront the psychological challenges associated with the loss of close others, physical decline, and, ultimately, our own death. In this talk, I’ll begin with a discussion of the psychological states, symptoms, and syndromes that accompany death, dying, and bereavement. This will address psychological symptoms commonly heightened among terminally ill patients and the significant others who care for and, most often, survive them. We will then review empirical tests of the controversial stages, or states, of grief both in dying patients facing their own death, as well as in their significant others before and after their loved one has died. We will review data demonstrating how peaceful acceptance – the emotional state of peacefulness -- coupled with cognitive acknowledgment of one’s impending death – has been linked to better end-of-life outcomes both for the dying patient (e.g., less burdensome care, better quality of death) and the bereaved survivor (lower rates of Posttraumatic Stress Disorder, Major Depressive Disorder, and Prolonged Grief Disorder). Finally, I will introduce our “Enhancing & Mobilizing the POtential for Wellness & Emotional Resilience of Caregivers of ICU Cancer Patients” (EMPOWER) psychosocial intervention, funded by the National Cancer Institute, as an approach designed to promote better end-of-life outcomes for critically ill patients and their loved ones alike. Preliminary findings will be presented, and future directions will be discussed.