Etiology Of Dementia Research Articles

The Relationship of APOE ε4, Race, and Sex on the Age of Onset and Risk of Dementia.

Objective: To investigate whether APOE ε4 genotype—an established risk factor for dementia—is associated with earlier age at diagnosis in addition to increased risk overall and in secondary analysis by race and sex.Methods: We followed up 13,782 dementia-free individuals (n = 10,137 White, n = 3,645 Black, baseline age 60–66 years) in the Atherosclerosis Risk in Communities study for up to 30 years. Dementia was operationalized using standardized algorithms incorporating longitudinal cognitive change, proxy report, and hospital or death certificate dementia codes. We used a mixture of generalized gamma distributions to simultaneously estimate time to dementia, time to dementia-free death, and the proportion of individuals with dementia, by APOE ε4 status (≥1 vs. no alleles).Results: Median age of dementia onset among APOE ε4 carriers was 81.7 (Blacks) and 83.3 years (Whites) compared with 82.6 (Blacks) and 85.7 years (Whites) in non-APOE ε4 carriers (p > 0.05 Blacks; p < 0.01 Whites). Age of dementia diagnosis did not differ by sex in ε4 carriers, but among non-carriers, average age was earlier in males than females regardless of race. APOE ε4 carriers had on average a higher proportion of diagnoses; results did not differ by race or sex.Conclusions: APOE ε4 carrier status is associated with earlier age of dementia diagnosis with differences across race and sex. These findings clarify the causal role of APOE in dementia etiology, which could help better identify at-risk subgroups and may help facilitate better research trial recruitment and design.

Psychopathology of Dementia: Psychology’s Pivotal Role

Biology does not completely explain dementia. We can neither predict nor confirm a diagnosis of dementia based purely on its biology. Recent studies looking at prevention using social interventions hold better promise for ameliorating the disease. Yet, we do not have a major theory to explain these outcomes without resorting to biology. By understanding that there are mediating and moderating psychological factors promoting dementia, we take a broader view of the disease than a simple binary approach. Psychology plays a vital role in this clinical disease, in how cognition affects dementia. The presumption is that all of cognition: perception, orientation, novelty, attention, the application of knowledge (praxis), calculation, language, abstract thinking, and memory can affect and bring about dementia. It is not dementia that causes cognitive decline but cognitive decline that causes dementia. The psychopathology of dementia can initiate dementia, moderate it by enhancing or retarding the progression of the disease or mediate the disease by acting as a confirmatory process. The tipping point expressed by apathy and depression heralds a change in cognition. The psychopathology of dementia is important in understanding the etiology of dementia as it holds the most promising avenue for curing some dementias.

An Integrative Literature Review on the Nomenclature and Definition of Dementia at a Young Age.

Background:There has been growing interest in young people living with dementia. Future research requires consensus on the terminology and operational definition of this group.Objective:The purpose of this integrative review was to explore and include all operational definitions used to define dementia at a young age.Methods:On August 14, 2020, the PubMed, Embase, Cinahl, and PsycInfo databases were searched for empirical and theoretical literature using Google. Various terms to describe and define ‘dementia’ and ‘at a young age’ were used to collect literature concerning terminology; age-related aspects, including cut-off ages and criteria; and etiologies of dementia at a young age.Results:The search yielded 6,891 empirical and 4,660 theoretical publications, resulting in the inclusion of 89 publications, including 36 publications containing an explicit discussion and 53 publications as confirmation. ‘Young-onset dementia’ was the most commonly used term of seven identified terms, in the last two decades. The age of 65 years at symptom onset was used most frequently when considering a total of six upper age limits and four criteria to define a cut-off age. Eight lower age limits and an option for subdivision based on age were included. We identified 251 different etiologies and 27 categories of etiologies.Conclusion:Despite relative consensus on the term young-onset dementia and an age at symptom onset being used as a cut-off criterion, much is still unclear concerning possible etiologies of dementia at a young age. In the current study, controversies were detected for discussion in an international consensus study.

ASSESSING THE EFFECTS OF RARE COPY NUMBER VARIANTS ON PSYCHIATRIC SYMPTOMS AND COGNITIVE ABILITY IN ∼1M INDIVIDUALS

The etiology of frontotemporal dementia (FTD) is poorly understood. To identify genes with predicted expression levels associated with FTD, we integrated summary statistics with external reference gene expression data using a transcriptome-wide association study approach.FUSION software was used to leverage FTD summary statistics (all FTD: n = 2154 cases, n = 4308 controls; behavioral variant FTD: n = 1337 cases, n = 2754 controls; semantic dementia: n = 308 cases, n = 616 controls; progressive nonfluent aphasia: n = 269 cases, n = 538 controls; FTD with motor neuron disease: n = 200 cases, n = 400 controls) from the International FTD-Genomics Consortium with 53 expression quantitative loci tissue type panels (n = 12,205; 5 consortia). Significance was assessed using a 5% false discovery rate threshold.We identified 73 significant gene–tissue associations for FTD, representing 44 unique genes in 34 tissue types. Most significant findings were derived from dorsolateral prefrontal cortex splicing data (n = 19 genes, 26%). The 17q21.31 inversion locus contained 23 significant associations, representing 6 unique genes. Other top hits included SEC22B (a gene involved in vesicle trafficking), TRGV5, and ZNF302. A single gene finding (RAB38) was observed for behavioral variant FTD. For other clinical subtypes, no significant associations were observed.We identified novel candidate genes (e.g., SEC22B) and previously reported risk regions (e.g., 17q21.31) for FTD. Most significant associations were observed in dorsolateral prefrontal cortex splicing data despite the modest sample size of this reference panel. This suggests that our findings are specific to FTD and are likely to be biologically relevant highlights of genes at different FTD risk loci that are contributing to the disease pathology.

Immune function, cortisol, and cognitive decline & dementia in an aging latino population

BackgroundThe etiology of dementias and cognitive decline remain largely unknown. It is widely accepted that inflammation in the central nervous system plays a critical role in the pathogenesis of dementia. However, less is known about the role of the peripheral immune system and interactions with cortisol, though evidence suggests that these, too, may play a role. MethodsUsing data from 1337 participants aged 60+ years from the Sacramento Area Latino Study of Aging (observational cohort) we investigated variation in trajectories of cognitive decline by pathogen IgG and cytokine levels. Linear mixed effects models were used to examine the association between baseline Interleukin (IL)−6, C-reactive protein, tumor necrosis factor (TNF)-α, and five persistent pathogens’ IgG response and trajectories of cognition over 10 years, and to examine interactions between immune biomarkers and cortisol. Stratified cumulative incidence functions were used to assess the relation between biomarkers and incident dementia. Inverse probability weights accounted for loss-to-follow-up and confounding. ResultsIL-6, TNF-α, and CMV IgG were statistically significantly associated with a higher log of Modified Mini-Mental State Examination errors (IL-6, β=0.0935 (95%CI: 0.055, 0.13), TNF-alpha β= 0.0944 (95%CI: 0.032, 0.157), and CMV, β= 0.0409 (95%CI: 0.013, 0.069)). Furthermore, cortisol interacted with HSV-1 and IL-6, and CRP for both cross-sectional cognitive function and rate of decline. No statistically significant relationship was detected between biomarkers and incidence of dementia. ConclusionsThese findings support the theory that the peripheral immune system may play a role in cognitive decline but not incident dementia. Furthermore, they identify specific markers amenable for intervention for slowing decline.

Current Alzheimer disease research highlights: evidence for novel risk factors.

Alzheimer disease (AD) is the most common type of dementia characterized by the progressive cognitive and social decline. Clinical drug targets have heavily focused on the amyloid hypothesis, with amyloid beta (Aβ), and tau proteins as key pathophysiologic markers of AD. However, no effective treatment has been developed so far, which prompts researchers to focus on other aspects of AD beyond Aβ, and tau proteins. Additionally, there is a mounting epidemiologic evidence that various environmental factors influence the development of dementia and that dementia etiology is likely heterogenous. In the past decades, new risk factors or potential etiologies have been widely studied. Here, we review several novel epidemiologic and clinical research developments that focus on sleep, hypoxia, diet, gut microbiota, and hearing impairment and their links to AD published in recent years. At the frontiers of AD research, these findings and updates could be worthy of further attention.

A-2 Clustering and Switching Indices as Discriminators between Alzheimer’s Dementia, Vascular Dementia, and Mild Cognitive Impairment on a Semantic Fluency Task

Abstract Objective Studies that have used semantic fluency tasks to guide differential diagnosis of Alzheimer’s disease (ad) and vascular dementia (VaD) typically only examine the total number of words produced, which has yielded conflicting results. The present study examined whether other indices of semantic fluency (i.e., clustering and switching), which are thought to better isolate the components of semantic memory and executive functioning abilities, would discriminate among ad, VaD, and mild cognitive impairment (MCI). Method A retrospective sample of 156 patients (mean age = 78.64; 76.3% female, 23.7% male; 26.9% White, 71.2% Black, 1.9% Other) who completed a comprehensive neuropsychological evaluation as part of a workup related to memory concerns and were diagnosed with ad, VaD, or MCI was utilized. Separate univariate analyses of variance were used to examine group differences on three indices of semantic fluency (animals): total words, mean cluster size, and number of switches. Results There was a significant main effect of group for total words [F(2,153) = 7.09, p = 0.001], mean cluster size [F(2, 153) = 3.44, p = 0.035] and number of switches [F(2,153) = 3.36, p = 0.037]. Bonferroni post-hoc tests revealed that the ad and VaD groups produced significantly fewer total words than the MCI group, the ad group produced significantly smaller clusters than the VaD group, and the VaD group produced significantly fewer switches than the MCI group. Conclusion Observed group differences suggest that clustering and switching may aid in discriminating between dementia etiologies. Future studies may benefit from examining the association between these fluency indices and performance on executive functioning and semantic knowledge tasks to better understand these findings.

Recent insights into Early Onset Dementia (EOD): A Review

The present study aims to review the prevalence and etiology of Early Onset Dementia (EOD) reflected in the population based studies worldwide .For this purpose, Bibliographic database searches and rigorous literature review were performed using the following keywords namely: “Dementia”, “Early onset dementia”, “Alzheimer’s disease” and “Senile Dementia” from the following databases: Pubmed, Medline between the years 2005 to 2019. The summary of report findings suggest that the prevalence of early onset dementia is reported to occur in 3-5% of the Indian population among predisposed individuals. This is an attempt to accumulate and collate in one spot all sort of multifactorial associations behind the pathogenesis of EOD in youth. These causes are Genetic change, Brain comorbidities, Alzheimer's ailment, vascular complications and increasingly other neuropsychiatric complications. We have made an attempt to analyze the pathogenesis of the early onset dementia in relation to their outcomes and a few manifestations which demonstrate the same. Future large-scale systematic reviews and network meta-analysis in this domain would facilitate dissemination of credible information with regards to the causative mechanism and possible therapeutic interventions and viable alternatives to possibly tackle and mitigate EOD.&#x0D; Keywords: Dementia, Early onset dementia, Alzheimer’s disease, Genetic alterations.

The Role of 18F-Flortaucipir (AV-1451) in the Diagnosis of Neurodegenerative Disorders.

Tau protein plays a vital role in maintaining the structural and functional integrity of the nervous system; however, hyperphosphorylation or abnormal phosphorylation of tau protein plays an essential role in the pathogenesis of several neurodegenerative disorders. The development of radioligand such as the 18F-flortaucipir (AV-1451) has provided us with the opportunity to assess the underlying tau pathology in various etiologies of dementia. For the purpose of this article, we aimed to evaluate the utility of 18F-AV-1451 in the differential diagnosis of various neurodegenerative disorders. We used PubMed to look for the latest, peer-reviewed, and informative articles. The scope of discussion included the role of 18F-AV-1451 positron emission tomography (PET) to aid in the diagnosis of Alzheimer’s disease (AD), frontotemporal dementia (FTD), dementia with Lewy bodies (DLB), and Parkinson’s disease with dementia (PDD). We also discussed if the tau burden identified by neuroimaging correlated well with the clinical severity and identified the various challenges of 18F-AV-1451 PET. We concluded that although the role of 18F-AV-1451 seems promising in the neuroimaging of AD, the benefit appears uncertain when it comes to the non-Alzheimer’s tauopathies. More research is required to identify the off-target binding sites of 18F-AV-1451 to determine its clinical utility in the future.

Les marqueurs biologiques des démences fronto-temporales

AbstractFrontotemporal lobar degeneration (FTLD) represents the second degenerative etiology of early-onset dementia after Alzheimer’s Disease. FTLD encompasses different phenotypes, notably the behavioural variant of frontotemporal dementia (bvFTD). FTLD can be frequently hereditary, molecular diagnosis should be performed facing family history of neurologic or psychiatric diseases, and even without any family history. Many genes are considered as pathogenic of FTLD and permit to classify cases as definite. C9ORF72, GRN and MAPT represent the main causative genes of FTLD. The determination of etiological markers of FTD, based on the nature of cerebral aggregates – TAU and TDP43 – was able to highlight variations between FTD patients and other cohorts. However, the great variability observed for these markers complicates a potential use in clinical practice for an individual diagnosis. The development of indirect markers is currently increasing, especially neurofilaments, and testifies that extensive research has been performed to better understand physiopathological processes underlying FTLD.

Lung Function Impairment and the Risk of Incident Dementia: The Rotterdam Study.

Background:The etiology of dementia may partly be underpinned by impaired lung function via systemic inflammation and hypoxia.Objective:To prospectively examine the association between chronic obstructive pulmonary disease (COPD) and subclinical impairments in lung function and the risk of dementia.Methods:In the Rotterdam Study, we assessed the risk of incident dementia in participants with Preserved Ratio Impaired Spirometry (PRISm; FEV1/FVC≥0.7, FEV1 < 80% predicted) and in participants with COPD (FEV1/FVC < 0.7) compared to those with normal spirometry (controls; FEV1/FVC≥0.7, FEV1≥80% predicted). Hazard ratios (HRs) with 95% confidence intervals (CI) for dementia were adjusted for age, sex, education attainment, smoking status, systolic blood pressure, body mass index, triglycerides, comorbidities and Apolipoprotein E (APOE) genotype.Results:Of 4,765 participants, 110 (2.3%) developed dementia after 3.3 years. Compared to controls, participants with PRISm, but not COPD, had an increased risk for all-type dementia (adjusted HRPRISm 2.70; 95% CI, 1.53–4.75; adjusted HRCOPD 1.03; 95% CI, 0.61–1.74). These findings were primarily driven by men and smokers. Similarly, participants with FVC% predicted values in the lowest quartile compared to those in the highest quartile were at increased risk of all-type dementia (adjusted HR 2.28; 95% CI, 1.31–3.98), as well as Alzheimer’s disease (AD; adjusted HR 2.13; 95% CI, 1.13–4.02).Conclusion:Participants with PRISm or a low FVC% predicted lung function were at increased risk of dementia, compared to those with normal spirometry or a higher FVC% predicted, respectively. Further research is needed to elucidate whether this association is causal and how PRISm might contribute to dementia pathogenesis.

Hypertension and Hypercholesterolemia Modify Dementia Risk in Relation to APOEɛ4 Status.

There is significant interest in understanding the role of modifiable vascular risk factors contributing to dementia risk across age groups. Risk of dementia onset was assessed in relation to vascular risk factors of hypertension and hypercholesterolemia among cognitively normal APOEɛ4 carriers and non-carriers. In a sample of prospectively characterized longitudinal cohort from the National Alzheimer's Coordinating Center database, 9,349 participants met criteria for normal cognition at baseline, had a CDR-Global (CDR-G) score of zero, and had concomitant data on APOEɛ4 status and medical co-morbidities including histories of hypertension and hypercholesterolemia. Multivariable Cox proportional hazards models adjusted for well-known potential confounders were used to compare dementia onset among APOEɛ4 carriers and non-carriers by young (≤65 years) and old (> 65 year) age groups. 519 participants converted to dementia within an average follow up of 5.97 years. Among older APOEɛ4 carriers, hypercholesterolemia was related to lower risk of dementia (HR (95% CI), 0.68 (0.49-0.94), p = 0.02). Among older APOEɛ4 non-carriers, hypertension was related to higher risk of dementia (HR (95% CI), 1.44 (1.13-1.82), p = 0.003). These results were corroborated among a subset with autopsy data characterizing underlying neuropathology. Among younger participants, vascular risk factors did not impact dementia risk, likely from a lower frequency of vascular and Alzheimer's as etiologies of dementia among this cohort. A history of hypercholesterolemia related to a lower risk of dementia among older APOEɛ4 carriers, while hypertension related to a higher risk of dementia among older APOEɛ4 non-carriers.

The role of NOTCH3 variants in Alzheimer's disease and subcortical vascular dementia in the Chinese population

Aims NOTCH3 gene mutations predominantly cause cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, a common etiology of subcortical vascular dementia (SVaD). Besides, there may be a pathogenic link between NOTCH3 variants and Alzheimer's disease (AD). We aimed to study the role of NOTCH3 variants in AD and SVaD patients.MethodsWe recruited 763 patients with dementia (667 AD and 96 SVaD) and 365 healthy controls from the Southern Han Chinese population. Targeted capture sequencing was performed on NOTCH3 coding and adjacent intron regions to detect the pathogenic variants in AD and SVaD. The relationship between common or rare NOTCH3 variants and AD was further analyzed using Plink1.9.ResultsFive known pathogenic variants (p.R182C, p.C201S, p.R544C, p.R607C, and p.R1006C) and two novel likely pathogenic variants (p.C201F and p.C1061F) were detected in 16 SVaD patients. Additionally, no pathogenic or likely pathogenic variants were found in AD patients. NOTCH3 was not associated with AD in either single‐variant association analysis or gene‐based association analysis.ConclusionOur findings broaden the mutational spectrum of NOTCH3 and validate the pathogenic role of NOTCH3 mutations in SVaD, but do not support the notion that NOTCH3 variation influences the risk of AD.

Visit-to-Visit Blood Pressure Variability, Neuropathology, and Cognitive Decline.

Large systolic blood pressure (SBP) variability has been proposed as a novel risk factor for dementia above and beyond SBP levels, but the underlying neuropathology is largely unknown. We investigated the relationship among visit-to-visit SBP variability, cognitive deterioration, and underlying neuropathologic changes. We used longitudinal data (between 2005 and 2019) from the National Alzheimer's Coordinating Center. A total of 13,284 dementia-free participants ≥50 years of age were followed up over a median of 5.0 (interquartile range 3.1-7.6) years. Neuropathology data were available in 1,400 autopsied participants. Visit-to-visit SBP variability was quantified from repeated annual SBP measurements. Cognitive deterioration was defined as conversion from normal cognition to mild cognitive impairment (MCI) or dementia or from MCI to dementia. Larger visit-to-visit SBP variability was associated with cognitive deterioration (adjusted odds ratio comparing extreme quintiles 2.64, 95% confidence interval 2.29-3.04, p < 0.001). It was also associated with a higher burden of vascular pathology (including microinfarcts, white matter lesions, atherosclerosis of the circle of Willis, and arteriolosclerosis) and with neurofibrillary tangle pathology assessed by Braak staging (all p < 0.05). The association with cognitive deterioration and vascular pathology appeared stronger among those with normal cognition vs those with MCI at baseline. These findings were observed after adjustment for age, sex, mean SBP, and other confounding variables. Similar results were observed for diastolic blood pressure variability. Larger visit-to-visit SBP variability was associated with cognitive deterioration. It was also associated with cerebrovascular pathology and neurofibrillary tangles. These results suggest the intertwined role of vascular and Alzheimer disease pathology in the etiology of dementia.

Beyond the average patient: how neuroimaging models can address heterogeneity in dementia.

Dementia is a highly heterogeneous condition, with pronounced individual differences in age of onset, clinical presentation, progression rates and neuropathological hallmarks, even within a specific diagnostic group. However, the most common statistical designs used in dementia research studies and clinical trials overlook this heterogeneity, instead relying on comparisons of group average differences (e.g. patient versus control or treatment versus placebo), implicitly assuming within-group homogeneity. This one-size-fits-all approach potentially limits our understanding of dementia aetiology, hindering the identification of effective treatments. Neuroimaging has enabled the characterization of the average neuroanatomical substrates of dementias; however, the increasing availability of large open neuroimaging datasets provides the opportunity to examine patterns of neuroanatomical variability in individual patients. In this update, we outline the causes and consequences of heterogeneity in dementia and discuss recent research that aims to tackle heterogeneity directly, rather than assuming that dementia affects everyone in the same way. We introduce spatial normative modelling as an emerging data-driven technique, which can be applied to dementia data to model neuroanatomical variation, capturing individualized neurobiological ‘fingerprints’. Such methods have the potential to detect clinically relevant subtypes, track an individual’s disease progression or evaluate treatment responses, with the goal of moving towards precision medicine for dementia.

Etiology of Dementia in Thai Patients

Introduction: Molecular imaging has been developed and validated in Thai patients, comprising a portion of patients in the dementia registry. This should provide a more accurate diagnosis of the etiology of dementia, which was the focus of this study. Methods: This was a multicenter dementia study. The baseline characteristics, main presenting symptoms, and results of investigations and cognitive tests of the patients were electronically collected in the registry. Functional imaging and/or molecular imaging were performed in patients with an equivocal diagnosis of the causes of dementia, especially in atypical dementia or young onset dementia (YOD). Results: There were 454 patients in the study. The mean age of the patients was 78 years, with 60% female. Functional imaging and/or molecular imaging were performed in 57 patients (57/454 patients, 13%). The most common cause of dementia was Alzheimer’s disease (AD; 50%), followed by vascular dementia (VAD; 24%), dementia with Lewy bodies (6%), Parkinson’s disease dementia (6%), frontotemporal dementia (FTD; 2.6%), progressive supranuclear palsy (2%), multiple system atrophy (0.8%), and corticobasal syndrome (0.4%). YOD accounted for 17% (77/454 patients), with a mean age of 58 years. The causes of YOD were early onset amnestic AD (44%), VAD (16%), behavioral variant FTD (8%), posterior cortical atrophy (6.5%), and logopenic variant primary progressive aphasia (5.2%). Conclusion: AD was the most common cause of dementia in Thai patients and the distribution of other types of dementia and main presenting symptoms were similar to previous reports in Western patients; however, the proportion of YOD was higher.

Circulating Inflammatory Proteins Associated with Dementia Risk in Older Adult Cancer Survivors in the Atherosclerosis Risk in Communities (ARIC) Study

Abstract Background Inflammation is linked to cognitive impairment (CI) in cancer survivors. But its role in survivors who develop dementia is unclear. Methods We evaluated dementia risk per log2 increase in 580 inflammatory proteins in 391 dementia-free long-term (&amp;gt;5 yrs) older adult survivors of prostate, breast, colorectal, endometrial and bladder cancers in ARIC. Plasma inflammatory proteins were measured at visit 5 (2011–13) using SomaScan, an aptamer-based assay. Participants were followed through visit 6 (2016–17). We adjusted for age, sex, race, years since cancer diagnosis, ApoE4, renal function, anti-inflammatory drug use and cancer/CVD shared risk factors. We also investigated proteins associated with dementia in 196 prostate and 135 breast cancer survivors, accounting for multiple testing by Bonferroni correction and false discovery rate Q-values. Results Survivors were 20% Black, 54% male, mean age of 76yrs, median time since diagnosis of 12yrs. 67 dementia cases occurred in 1780 person-yrs. After FDR correction, 73 proteins were statistically significantly associated with dementia risk. TMEM87B, CD9, RAF1, IL21sR and FGF7 showed the strongest positive association, with HR:3.4–3.8 per Δlog2. LAIR1, IL36B, FGFR3, FLRT3 and LSAMP showed the strongest inverse association, HR:0.1–0.2. Only syntaxin12 (STX12) was significant after Bonferroni correction, HR:2.2. Associations of some inflammatory proteins with dementia were cancer site-specific. In breast cancer survivors, IL6, HMGA2, IFN-GR1, SAP, TNFRSF1a, TNFRSF14, and TNFAIP3, were associated with dementia. STX12 and RAF1 were significantly associated (q &amp;lt;0.05) with dementia in all, prostate, and breast cancer survivors. Conclusion Inflammatory proteins were associated with dementia in older adult cancer survivors, including STX12 (enriched in brain, linked to WNT signaling loss, exerts CNS effects) and RAF1 (regulates MAPK/ERK pathway, previously identified in dementia etiology). Inflammatory proteins previously associated with CI, including TNF proteins/receptors, were associated with dementia in breast cancer survivors. If confirmed, these proteins may warrant evaluation as potential biomarkers for dementia risk screening, and possibly preventive/therapeutic targets in cancer survivors. Funding: NHLBI, NCI, NPCR

How do delirium motor subtypes differ in phenomenology and contributory aetiology? a cross-sectional, multisite study of liaison psychiatry and palliative care patients

ObjectivesTo investigate whether delirium motor subtypes differ in terms of phenomenology and contributory aetiology.DesignCross-sectional study.SettingInternational study incorporating data from Ireland and India across palliative care, old age liaison psychiatry and...

Socio-demographic and clinical features of patients with dementia attended in the psychiatry department

IntroductionDementia’s prevalence increases due to population aging, it has become a major public health concern.ObjectivesTo estimate the incidence of dementia and to describe the socio-demographic and clinical profile of patients attended in the psychiatry department of Gabes (Southern of Tunisia).MethodsIt was a retrospective descriptive study including all the patients who attended for the first time in the psychiatry department of Gabes, from the 1st January, 2010 to December 31, 2018, and who were diagnosed with dementia according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Socio-demographic and clinical data were assessed. The Mini Mental State Examination (MMSE) was used as a neuropsychological examination.ResultsWe included 98 patients. The mean annual hospital incidence of dementia was 2.38%. The mean age was 76.5 ± 9.8 years. Patients were married (68%), illiterate (68%) and jobless (42.9%). A family history of dementia was noted in 39.8% of patients. The common cardiovascular comorbidity was high blood pressure (41.8%). Among our patients, 30 (30.6%) were smokers. The mean age of onset of dementia was 73 ± 11 years. The mean duration of untreated dementia was 3 years [3 months to 11 years]. First symptoms were mainly memory disorders (57.3 %) and behavioral disorders (17.3%) The mean MMSE score was 14 ± 4.8. Alzheimer’s disease was the most frequent etiology of dementia (80 cases, 82.7%).ConclusionsOur study shows a high incidence of dementia and made it possible to draw up a socio-demographic and clinical profile of dementia patients.DisclosureNo significant relationships.

Criminal behavior in frontotemporal dementia and Alzheimer's disease

Seniorenkriminalität ist insgesamt ein seltenes Phänomen. Bei älteren Straftätern hat es die Justiz in hohem Maß mit Ersttätern zu tun, die mehrheitlich männlichen Geschlechts sind. Eine mögliche Ursache von Erstkriminalität im höheren Lebensalter stellen Demenzerkrankungen dar. Es ist jedoch wenig dazu bekannt, wie häufig Demenzerkrankungen tatsächlich Ursache delinquenten Verhaltens im höheren Lebensalter sind. Die Demenzprävalenz in Studien mit forensischen Kohorten älterer Straftäter ist sehr heterogen, was vor allem studienmethodisch begründet ist. Längsschnittlich begehen etwa 50 % aller Patienten mit frontotemporaler Demenz und etwa 10 % aller Patienten mit Alzheimer-Demenz Delikte im Erkrankungsverlauf. Die neurobiologischen Entstehungsmechanismen von Delinquenzverhalten im Rahmen von Demenzen sind unvollständig verstanden. Nach aktuellen Erkenntnissen wird davon ausgegangen, dass Erstdelinquenz im Rahmen von Demenzerkrankungen als Folge von Beeinträchtigungen der sozialen Kognition, Empathiefähigkeit und der Verhaltenskontrolle zu verstehen ist. Bedeutsam sind insbesondere frontale und anteriore temporale Hirnstrukturen. Demenzerkrankungen können zu Beeinträchtigungen der Schuldfähigkeit führen, weshalb forensisch-psychiatrische Sachverständige auch mit Demenzerkranken konfrontiert sind. Hierbei müssen ätiologiespezifische Besonderheiten berücksichtigt werden. Insbesondere Erstdelikte im Rahmen wesensuntypischer Persönlichkeitsänderungen nach dem 50. Lebensjahr sollten an eine neurodegenerative Ätiologie denken lassen. Insbesondere frontotemporale Demenzerkrankungen, wie die behaviorale Variante einer frontotemporalen Demenz (bvFTD), aber auch die semantische Demenz (svPPA), prädisponieren zu delinquentem Verhalten.Diese Arbeit fasst aktuelle Erkenntnisse zu dieser forensisch-psychiatrisch, aber auch klinisch relevanten Thematik zusammen.