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Memory and cognition are critical parts of who we are. Our capacity for recall allows us to use past experience to guide our actions. Our cognitive abilities allow us to monitor events and evaluate plans for action. In aging there are varying degrees of decline in cognitive function which begin in the 30s and are quite common. They are not a disease and are accompanied by the growth of wisdom which can negate the influence of age-related memory changes. Memory losses with aging can be avoided with consideration of the importance of attention for memory. The role of forgetting as a normal activity of the brain is critical. It is necessary to realize that the influences of aging and age-related disease (such as Alzheimer’s) on brain function are not determined only on the processes of aging and disease -- the effect of these processes on our performance abilities depends upon our cognitive, physical, psychological, and social reserves. We all need to enhance these reserve capacities to decrease the influence of the aging process and developing brain disease on our function. This chapter reviews the functions of memory and how losses that accompany aging can best be managed.
The neurodegenerative diseases Alzheimer’s, Parkinson’s, frontotemporal lobar degeneration, Lewy body disease, and amyotrophic lateral sclerosis are all age-related and caused by genes in only 1-10 percent of cases. Dementia describes a syndrome in which there are cognitive difficulties including impaired memory, judgment, planning, language, and other deficits. Alzheimer’s is the commonest cause of dementia. In the brain in neurodegenerative diseases there is abnormal folding of proteins creating thread-like filaments called amyloid. There is also abnormal activation of inflammation with free radicals and harmful cells. There are things we can do regarding diet and other actions that can lower the risk of developing neurodegenerative diseases with aging. High levels of physical and mental activity throughout life along with attention to a healthy plant-based diet can enhance our four reserves and diminish amyloid deposition and overactivity of the immune system. Lifestyle measures can also protect us from the effect of brain pathologies that may develop. There are many causes of memory loss other than Alzheimer’s disease which are completely reversible when properly recognized.
Risk factors for Alzheimer’s disease, such as cardiovascular, metabolic and inflammatory problems, were probably less prevalent throughout much of human history compared to today in post-industrial societies. Therefore, I explore the possibility that individuals today have greater Alzheimer’s disease risk compared to our age-matched, pre-modern counterparts. Additionally, a critical way in which human physiology has changed across history relates to dramatic changes in female reproductive life history norms. Reproductive life history may exert cumulative effects across an individual’s lifespan, bestowing considerable influence on geriatric disease risk. A growing body of research links women’s reproductive life histories with Alzheimer’s disease risk. Here, I briefly discuss ways in which aspects of female reproductive life history (e.g. reproductive span, pregnancy and breastfeeding) might alter physiological pathways implicated in Alzheimer’s disease aetiology, as well as how each of these aspects of female reproductive life history have shifted across our species’ evolutionary past. I also explore the connections between the apolipoprotein E gene, its context-dependent role in Alzheimer’s disease risk and its emerging role in women’s reproductive function. In summary, some aspects of pre-modern female reproductive life history patterns could indicate lower age-matched risk in the past, but further research is needed to establish the relevant biological pathways and epidemiological patterns.
Loss of empathy is a hallmark feature of behavioral variant frontotemporal dementia (bvFTD). Change in socioemotional functioning identified by others is often the primary initial presenting concern in this disorder, in contrast to more subtle early cognitive changes and limited patient insight. The present study examined the predictive utility of an empathy informant-report measure for discriminating clinician-diagnosed bvFTD from other dementia syndromes.
Data from the National Alzheimer’s Coordinating Center (NACC) database were used to study individuals with bvFTD (n = 406) and other dementia syndromes (n = 385). Participants were administered neuropsychological measures and collateral informants completed an informant-report of empathy.
Informants reported that patients with bvFTD demonstrated significantly lower levels of empathic concern [F(1, 789) = 120.91, p < .001, η2 = 0.13] and perspective taking [F(1, 789) = 153.08, p < .001, η2 = 0.16] than patients with other dementia syndromes. These differences were not attributable to the level of global cognitive impairment. Empathy scores were not significantly associated with any neurocognitive measure when controlling for age. ROC curve analyses showed fair to good clinical utility of the informant-report empathy measure for distinguishing bvFTD from non-bvFTD, whereas a traditional measure of executive functioning failed to differentiate the groups.
These findings indicate that informant ratings of empathy offer a unique source of clinical information that may be useful in detecting neurobehavioral changes specific to bvFTD before a clear neurocognitive pattern emerges on testing.
Depression is an important, potentially modifiable dementia risk factor. However, it is not known whether effective treatment of depression through psychological therapies is associated with reduced dementia incidence. The aim of this study was to investigate associations between reduction in depressive symptoms following psychological therapy and the subsequent incidence of dementia.
National psychological therapy data were linked with hospital records of dementia diagnosis for 119808 people aged 65+. Participants received a course of psychological therapy treatment in Improving Access to Psychological Therapies (IAPT) services between 2012 and 2019. Cox proportional hazards models were run to test associations between improvement in depression following psychological therapy and incidence of dementia diagnosis up to eight years later.
Improvements in depression following treatment were associated with reduced rates of dementia diagnosis up to 8 years later (HR = 0.88, 95% CI 0.83–0.94), after adjustment for key covariates. Strongest effects were observed for vascular dementia (HR = 0.86, 95% CI 0.77–0.97) compared with Alzheimer's disease (HR = 0.91, 95% CI 0.83–1.00).
Reliable improvement in depression across psychological therapy was associated with reduced incidence of future dementia. Results are consistent with at least two possibilities. Firstly, psychological interventions to improve symptoms of depression may have the potential to contribute to dementia risk reduction efforts. Secondly, psychological therapies may be less effective in people with underlying dementia pathology or they may be more likely to drop out of therapy (reverse causality). Tackling the under-representation of older people in psychological therapies and optimizing therapy outcomes is an important goal for future research.
Aging is a subject of concern to everyone, but is widely misunderstood. If we view it as inevitable, we miss the fact that not everyone is able to grow to an old age. Realization of this reality helps us to understand that aging presents a wonderful opportunity - an opportunity to make choices about how we live which can enhance the aging process and offer a chance to live to our potential. This book clearly presents the four, multiple reserve, factors (cognitive, physical, psychological and social) which impact our ability to have healthy responses to the stresses of aging. By giving the biological basis for the advice given, you will learn the steps to take in your activities, diet and mental outlook to grasp the opportunity that aging offers. Everyone must know that what we do makes a difference.
Dementia, a slowly progressive disease, is poorly diagnosed. One reason is that it is difficult to use the screening tools. The six-item cognitive impairment test (6-CIT) is brief, with six items, and has a confirmed scoring system that can easily be used by an average individual. This review aimed to analyze the predictive validity of the 6-CIT including comparisons with other tools such as the Mini-Mental State Examination (MMSE).
Literature searches were performed on the MEDLINE, EMBASE, CINAHL, and PsycArticles using the dementia and 6-CITas keywords. The Quality Assessment of Diagnostic Accuracy Studies-2 was applied to assess the risk of bias.
Seven studies with 6,831 participants that met the selection criteria were included. The pooled sensitivity of the 6-CIT analyzed in seven studies was 0.82 (95% CI 0.73–0.89), the pooled specificity was 0.87, and the summary receiver operating characteristic (sROC) curve was 0.90 (SE = 0.04). The diagnostic performance of the 6-CIT and MMSE was compared in three studies. The pooled sensitivity of the 6-CIT was 0.85, the pooled specificity was 0.91, and the sROC curve was 0.91, whereas the MMSE values were 0.70, 0.93, and 0.68, respectively.
This review presents evidence that the 6-CIT has excellent dementia screening performance and could be used as a potential alternative to the MMSE. The 6-CIT may provide an opportunity for early detection of dementia.
A previously healthy woman began to present recurrent episodes of reduplicative paramnesia within her home and later structured visual hallucinations. The case was initially oriented as an incipient vascular dementia. Detailed anamnesis and neuropsychological examination suggested a rapidly progressive pattern of neuropsychological deficits mostly attributable to parieto-occipital disturbances with some component of fronto-temporal involvement. Subsequently, cerebellar symptoms were added. Although the initial imaging studies were inconclusive, the MRI performed during follow-up showed a series of findings compatible with a prion disease. Based on the neuropsychological and clinical features and the imaging pattern, the diagnosis of Heidenhain Variant of Creutzfeldt-Jakob disease was established. This is the first report of a Heidenhain Variant of Creutzfeldt-Jakob disease presenting as a reduplicative paramnesia as the first manifestation of this disease.
Serial position scores on verbal memory tests are sensitive to early Alzheimer’s disease (AD)-related neuropathological changes that occur in the entorhinal cortex and hippocampus. The current study examines longitudinal change in serial position scores as markers of subtle cognitive decline in older adults who may be in preclinical or at-risk states for AD.
This study uses longitudinal data from the Religious Orders Study and the Rush Memory and Aging Project. Participants (n = 141) were included if they did not have dementia at enrollment, completed follow-up assessments, and died and were classified as Braak stage I or II. Memory tests were used to calculate serial position (primacy, recency), total recall, and episodic memory composite scores. A neuropathological evaluation quantified AD, vascular, and Lewy body pathologies. Mixed effects models were used to examine change in memory scores. Neuropathologies and covariates (age, sex, education, APOE e4) were examined as moderators.
Primacy scores declined (β = −.032, p < .001), whereas recency scores increased (β = .021, p = .012). No change was observed in standard memory measures. Greater neurofibrillary tangle density and atherosclerosis explained 10.4% of the variance in primacy decline. Neuropathologies were not associated with recency change.
In older adults with hippocampal neuropathologies, primacy score decline may be a sensitive marker of early AD-related changes. Tangle density and atherosclerosis had additive effects on decline. Recency improvement may reflect a compensatory mechanism. Monitoring for changes in serial position scores may be a useful in vivo method of tracking incipient AD.
Mild cognitive impairment (MCI) represent a state of cognitive function between normal aging and dementia and does not always progress to dementia. Neuroinflammation has a key role in the pathogenesis of neurodegeneration. Determining the associations of neuroinflammatory markers in the blood with clinical disease severity may be useful for early diagnosis of cognitive impairment and prediction of the development of severe dementia.
The aim of our study was to compare the serum concentration of a panel of inflammatory markers in patients with MCI and dementia as well as their associations with clinical symptoms.
Patients were evaluated using Mini-Mental State Examination (MMSE), Clock Drawing Test (CDT), Montreal Cognitive Assessment scales (MoCA), Clinical Dementia rating (CDR) and Hospital Anxiety Depression Scale (HADS). We determined the serum concentration of a panel of inflammatory markers (25 units) cytokines, chemokines, growth factors and several others on Mulliplex and prepared multivariate analysis to investigate associations between clinical features and serum concentration.
Patients with dementia had lower scores on scales than the control and MCI groups. MCI patients were equal to the control group, except for the MMSE scale. EGF, eotaxin-1, GRO-α, IP-10, IL-8, MIP-1β, sCD40L, TNF-α, MDC and MCP-1, VEGF were differ between groups. Multivariate analysis identified some neuroinflammatory parameters associated with the severity of the disease.
We identified some neuroinflammatory parameters associated with dementia and MCI. Many of them have been poor described and data is contradictory. It is necessary to investigate these parameters as potential biomarkers of neurodegeneration in further studies.
Agitated behaviors is a common neuropsychiatric symptom (NPS) in dementia, defined as inappropriate verbal, vocal, or motor activity that is not thought to be caused by an unmet need. It is frequently reported as a major problem, that impairs the quality of life for the elderly themselves and for caregivers. There has been increasing interest in the use of sedative antidepressants to treat NPS due to concerns over the safety and efficacy of antipsychotics in this setting.
We aim to review clinical evidence of alternatives to antipsychoticst to manage agitation in dementia.
We conduct a non-systematic review of recent evidence on dementia and agitation, using PubMed/Medline database.
Although non-pharmacological interventions are the first-line treatment for agitation, it is a legitimate target for therapeutic intervention and according to previous guidelines, antipsychotic are among the most used drugs, albeit restricted because of side-effects. A substitution strategy to avoid antipsychotic prescription was highly considered, however there is limited evidence to support the use of antidepressants as a safe and effective alternative for agitation in dementia. Studies compare Mirtazapine, Selective serotonin reuptake inhibitors (SSRIs) and Trazodone and a reduced benefit in mortality is observed. However, citalopram was more effective were more likely outpatients for moderately agitation and Mirtazapine reveals being potentially harmful, in different studies.
Moving forward, a greater understanding of NPS neurobiology, will help to clarify the efficacy of Antedepressants for the treatment of agitation in dementia. Benefits an also the patient and caregiver preference should be kept in mind.
Traumatic brain injury (TBI) may alter dementia progression, although co-occurring neuropsychiatric symptoms (NPS) have received less attention. The mild behavioral impairment (MBI) construct relates NPS to underlying neural circuit disruptions, representing an important area of inquiry regarding TBI and dementia.
(1) to examine the influence of prior TBI history (preceding study enrollment) on MBI incidence in all-cause dementia (prior to dementia diagnosis, i.e. MBI’s original definition) and (2) to utilize MBI domains as a construct for examining the influence of TBI on related NPS across the course of dementia onset and progression.
Using National Alzheimer’s Coordinating Center data, individuals progressing from normal cognition to all-cause dementia over 7.6±3.0 years were studied to estimate MBI incidence and symptom domains in 124 participants with prior TBI history compared to 822 without.
Moderate-severe TBI was associated with the social inappropriateness MBI domain (ORadj.=4.034; p=0.024) prior to dementia onset, and the abnormal perception/thought content domain looking across dementia progression (HRadj.=3.703,
p=0.005). TBI (all severities) was associated with the decreased motivation domain looking throughout dementia progression (HRadj.=1.546,
TBI history is associated with particular MBI domains prior to onset and throughout progression of dementia. Understanding TBI’s impact on inter-related NPS may help elucidate underlying neuropathology.
During the last decades, the incidence of syphilis is on the rising, particularly in the United States of America and Europe. Neurosyphilis is a disease that has a vast differential diagnostic. With that in mind, clinicians have some difficulties to identify it rapidly. A case of a 57-year-old man is presented, with a brutal change in his behavior, associated with a dementia-like syndrome. He is diagnosed with neurosyphilis.
The main goal is to present his clinical psychiatric symptoms and diagnosis procedure, the treatment that he received and his clinical outcome in the psychogeriatric department.
The treatment was based in an integrated framework of pharmacology and psychotherapy.
The patient was able to slowly recover and to get back home, we a solid structure to make the follow up.
This clinical vignette represents a growing number of adult patients that present themselves for the first time with dementia-like symptoms. It is important to remember, that many diseases are capable of mimicking dementia and their exclusion before admitting a diagnosis of dementia is mandatory.
The behavioural variant of frontotemporal dementia (bvFTD) is a devastating neurodegenerative syndrome with its peak in the early sixties at about 13 per 100,00. The diagnosis of bvFTD relies on clinical assessment as patients present executive and behavioural deficits, like apathy, loss of motivation and personality changes. Current diagnosis criteria lack specificity and symptomatic overlap between bvFTD and primary psychiatric disorders (PPD) pose a diagnostic conundrum, with half of bvFTD patients previously receiving a psychiatric diagnosis.
The goal is to discuss the syntomatic overlap of these two entities.
Brief non-systematic literature review on the topic, illustrated by a case-report presentation.
A 69 year old men, retired and single, is committed for thought and behavior disorganization and insomnia. He presented expansive mood but also temporal and spatial disorientation and periods of incongruous speech. This patient’s clinical presentation could both entice a diagnosis of bvFTD but also of an affective disorder, especially since it has been reported that neuropsychiatric presentations, like late-onset psychosis or mania, can be the initial presentation of this form of dementia, particularly in patients with C9orf72 mutations, who often display persecutory or grandiosity delusions.
This clinical case exemplifies the difficulty that lies in differentiating cases of bvFTD from late-onset idiopathic mood or psychotic disorders. It is important to consider that on cognitive assessment patients with bvFTD score significantly worse on executive function tests that PPD patients No disease- modifying therapies are available for patients with bvFTD, therefore drug treatment should focus on the most disruptive or taggable behaviours.
Sexuality is one of the basic needs in human life and its positive effects for the wellbeing are undeniable. People with dementia, despite cognition and functioning impairments, still pursue intimacy as part of their expression of basic human instincts.
We aim to address the subject of sexuality among patients with dementia, emphasizing the physiological, environmental and legal barriers.
We conduct a non-systematic review of recent evidence on dementia and sexuality, using PubMed/Medline database.
People with dementia face several difficulties expressing their sexuality. First, they struggle with physiological barriers to enjoyment of sexuality, such as ageism, apathy and limited free mobility. Secondly, either at home or in long-term care facilities, privacy is usually abolished. For care facilities, the Sexuality Assessment Tool supports the normalization of sexuality and self-audit policies that promote resident rights for privacy and assistance. Moreover, expression of sexuality in elderly can be misinterpreted as disinhibition, leading to unnecessary use of psychotropics to cease these behaviors. Additionally, legal barriers regarding consent arise when a partner loses the ability to consent sexual activity, questioning agreement and mutual desire. The Lichtenberg and Strzepek Decision Tree for Capacity to Participate in Intimate Relationships can be helpful to address this issue.
Sexuality in older people remains neglected in clinical intervention. Besides the urgent need to deconstruct stereotypes, families and staff must be sensitized to understand the changes in expression and perception of sexuality among people with dementia, rather than being indifferent or medicate what can be perceived as disinhibited/distorted expressions of normal needs.
Late onset stress symptomatology (LOSS) is a relatively new concept in combat veterans, which includes repeated but not intrusive thoughts about combat-related experiences, irritability, or nightmares that do not cause impairment of daily functioning.
The objectives of this study were to identify the LOSS phenomenon in geriatric combat veterans and to establish a correlation between LOSS and cognitive deficit ± major stressors.
The electronic database was searched for the last 2 years from starting the study with the hypothesis that the LOSS phenomenon has been diagnosed with sleep, anxiety, trauma-related, or impulse control related disorders. Records were examined for trauma-related symptoms, excluding major symptoms of trauma-related stressors. The veterans were assessed objectively using LOSS, PCL-5 (PTSD checklist for DSM-5), social readjustment rating scales, and MOCA (Montreal Cognitive Assessment scale) for cognitive screening.
We reviewed 1329 patient records and identified 35 potential LOSS subjects. Four veterans were diagnosed with PTSD not otherwise specified, 2 with anxiety disorder unspecified, and 1 veteran with nightmare disorder. The majority (85%) of the veterans scored >40 in PCL-5, and only one veteran fulfilled the criteria for LOSS, who scored 67 on the LOSS scale. All the veterans scored ≤25 on MOCA with a significant deficit in recent recall.
Our study shows new onset stress-related symptoms are strongly associated with significant cognitive deficits and higher individual stress levels. The onset of PTSD symptoms in older combat veterans might have been correlated with the onset of cognitive deficits, as suggested by several other studies.
Dementia develops slowly and insidiously and causes cognitive impairment. The diagnosis is pivotal for relevant treatment and care. However, 50,000 people are estimated to have undiagnosed dementia in Denmark, while 36,000 are diagnosed.
The municipalities offers a home visit to the population at the ages of 75 and 80 years to assess the need of care and prevent sickness. These home visits are well established and might offer an unused opportunity to detect cognitive impairment and dementia.
To assess impaired cognition at home visits in order to initiate clinical examination for dementia.
A feasibility study with the use of Brief Assessment of Impaired Cognition Questionnaire (BASIC-Q) (sensitivity 0.92, specificity 0.97) at home visits. It is expected to include 1000 participants without a dementia diagnosis at the ages of 75 and 80 years. Participants will be included in a period of 12 moths (in the year of 2022), in a number of municipalities.
If the screening for cognitive impairment is positive, the participant is motivated for clinical examination at the general practitioner. Follow-up through registers and general practitioners.
Preliminary results will be presented at the conference.
Assessment of cognition might give an opportunity to start medication and social support early in the elderly with impaired cognition and undiagnosed dementia.
Obsessive-compulsive symptoms (OCS) have been described in many neurological disorders, including dementia. A meta-analysis by the authors (2021) reported a prevalence of OCS in dementia of approx. 35.8%, and a higher percentage in frontotemporal dementia (FTD) (46.7%). The literature also points that obsessive-compulsive disorder with late-life onset is rare, but those cases are frequently associated with neurologic injury, and some authors suggest a role of cognitive disfunction.
Our main goal was to describe the neurobiologic and cognitive underpinnings of OCS in patients with dementia.
MEDLINE, CENTRAL and PsycNet databases were searched for articles about obsessive-compulsive symptoms in dementia. Search terms included “obsessive”, “compulsive”, “OCD”, “cognitive decline”, “cognitive dysfunction” and “dementia”. Titles, abstracts and full texts were screened independently by 2 reviewers.
Correlations between dysfunction / lesions in various circuits in the context of dementia and OCS were found, such as (1) frontal regions (specially the orbitofrontal cortex) and anterior cingulate cortex (2) fronto-striatal-thalamic circuits (3) temporal structures; (4) cerebellar structures; (5) serotoninergic, dopaminergic, and cholinergic neurotransmission. A high proportion of studies concerned FTD. Regarding cognitive mechanisms, there is a focus on the importance subjective concerns about cognitive functioning, which could exacerbate obsessional beliefs and maladaptive responses to intrusions.
The main brain circuits implicated in dementia, specially FTD, and OCS are those involving frontal regions and the fronto-striatal-thalamic circuits, with areas such as the temporal and cerebellar structures algo being studied. The correlation between dysfunctional circuits in dementia and OCS could give us new hints about OCD and its treatment.