Criminal Behavior in the Four Years Preceding Diagnosis of Neurocognitive Disorder : A Nationwide Register Study in Finland

Objective: To explore the criminality of patients with subsequent diagnosis of Alzheimer's disease (AD), frontotemporal dementia (FTD), or Lewy body dementias (LBD) in the four years preceding diagnosis. Design: Nationwide register study. Setting: Data on Finnish patients were collected from the discharge register and data on criminal offending from the police register. Research findings were compared with the same-aged general population. Participants: A total of 92,191 patients who had received a diagnosis of AD (N = 80,540), FTD (N = 1,060), and LBD (N = 10,591) between 1998 and 2015. Measurements: Incidences and types of crimes, the standardized criminality ratio (number of actual crimes per number of expected crimes), and the numbers of observed cases and person-years at risk counted in five-year age groups and separately for both genders and yearly. Results: At least one crime was committed by 1.6% of AD women and 12.8% of AD men, with corresponding figures of 5.3% and 23.5% in FTD, and 3.0% and 11.8% in LBD. The first crime was committed on average 2.7 (standard deviation 1.1) years before the diagnosis. The standardized criminality ratio was 1.85 (95% confidence interval [CI] 1.43 -2.37) in FTD women and 1.75 (95% CI 1.54-1.98) in FTD men, and in AD 1.11 (95% CI 1.04-1.17) and 1.23 (95% CI 1.20-1.27), respectively. Traffic offences and crimes against property constituted 94% of all offences. Conclusion: Criminal acts may occur several years prior to the diagnosis of dementia. If novel criminality occurs later in life, it may be associated with neurocognitive disorder.Peer reviewe

Regional structural hypo- and hyperconnectivity of frontal-striatal and frontal-thalamic pathways in behavioral variant frontotemporal dementia

Behavioral variant frontotemporal dementia (bvFTD) has been predominantly considered as a frontotemporal cortical disease, with limited direct investigation of frontal–subcortical connections. We aim to characterize the grey and white matter components of frontal–thalamic and frontal–striatal circuits in bvFTD. Twenty‐four patients with bvFTD and 24 healthy controls underwent morphological and diffusion imaging. Subcortical structures were manually segmented according to published protocols. Probabilistic pathways were reconstructed separately from the dorsolateral, orbitofrontal and medial prefrontal cortex to the striatum and thalamus. Patients with bvFTD had smaller cortical and subcortical volumes, lower fractional anisotropy, and higher mean diffusivity metrics, which is consistent with disruptions in frontal–striatal–thalamic pathways. Unexpectedly, regional volumes of the striatum and thalamus connected to the medial prefrontal cortex were significantly larger in bvFTD (by 135% in the striatum, p = .032, and 217% in the thalamus, p = .004), despite smaller dorsolateral prefrontal cortex connected regional volumes (by 67% in the striatum, p = .002, and 65% in the thalamus, p = .020), and inconsistent changes in orbitofrontal cortex connected regions. These unanticipated findings may represent compensatory or maladaptive remodeling in bvFTD networks. Comparisons are made to other neuropsychiatric disorders suggesting a common mechanism of changes in frontal–subcortical networks; however, longitudinal studies are necessary to test this hypothesis.Miller Family Bridgewater Illawarra Health and Medical Research Initiative Summer Scholarship; The Swedish Alzheimer foundation; Thureus foundation; The Swedish Society for Medical Research; The Bente Rexed Gersteds Foundation for Brain Researc

Longitudinal decreases in multiple cerebrospinal fluid biomarkers of neuronal injury in symptomatic late onset Alzheimer\u27s disease

INTRODUCTION: Individuals in early stages of Alzheimer\u27s disease are a targeted population for secondary prevention trials aimed at preserving normal cognition. Understanding within-person biomarker(s) change over time is critical for trial enrollment and design. METHODS: Longitudinal cerebrospinal fluid samples from the Alzheimer\u27s Disease Neuroimaging Initiative were assayed for novel markers of neuronal/synaptic injury (visinin-like protein 1, Ng, and SNAP-25) and neuroinflammation (YKL-40) and compared with β amyloid 42, tau, and phospho-tau181. General linear mixed models were used to compare within-person rates of change in three clinical groups (cognitively normal, mild cognitive impairment, and Alzheimer\u27s disease) further defined by β amyloid status. RESULTS: Levels of injury markers were highly positively correlated. Despite elevated baseline levels as a function of clinical status and amyloid-positivity, within-person decreases in these measures were observed in the early symptomatic, amyloid-positive Alzheimer\u27s disease group. DISCUSSION: Knowledge of within-person biomarker change will impact interpretation of biomarker outcomes in clinical trials that are dependent on disease stage

Neurofilament light chain: a biomarker for genetic frontotemporal dementia

Objective: To evaluate cerebrospinal fluid (CSF) and serum neurofilament light chain (NfL) levels in genetic frontotemporal dementia (FTD) as a potential biomarker in the presymptomatic stage and during the conversion into the symptom

Causas, aparición, frecuencia y tratamientos de las conductas agresivas en pacientes con demencia tipo Alzheimer: una revisión bibliográfica

Trabajo de Grado en Psicología, curso 2018-2019[ES] Se espera que la supervivencia en la población general de mayores de 60 años se duplique para el año 2050, situándose en el 22% según el INE. Actualmente uno de cada cuatro hogares españoles se ve afectado por un familiar con Alzhéimer, según la Confederación Española de Alzheimer (CEAFA). El objetivo de este trabajo es tratar de analizar y exponer la información más actualizada sobre las conductas agresivas en la enfermedad de Alzheimer (EA), ya que es uno de los síntomas que más preocupa a cuidadores y familiares. La metodología a seguir es mediante la revisión bibliográfica de 21 artículos obtenidos a través de fuentes científicas. Los resultados muestran en primer lugar que las conductas agresivas en la EA son multicausales, teniendo un mayor peso los síntomas depresivos y psicóticos. En segundo lugar se observó como la aparición de las agresiones aumenta a medida que se agrava la enfermedad siendo menos frecuentes al inicio. En cuanto a los tratamientos actuales los más eficaces son los farmacológicos, y nuevas terapias alternativas que contribuyen a un mejor enfoque de los síntomas. Es importante que se continúe investigando en esta línea para poder afrontar las conductas agresivas de los pacientes con EA de una forma más adecuada y reducir el impacto que supone para pacientes, cuidadores y familiares. [EN] Survival in general population will increase twofold in 2050, reaching 22% taking into consideration the data from the INE (National Statistics Institute, Spain). Currently, one out of every four Spanish households has a relative stricken with Alzheimer’s, according to the Spanish Alzheimer’s Confederation (CEAFA). The aim of this project is to try to analyze and expose the most current information on aggressive behaviors in Alzheimer’s disease (AD), inasmuch as it is one of the most worrisome symptoms for caregivers and family members. The methodology that have followed is based on the bibliographic review of 21 articles obtained through scientific sources. The results show, firstly, that aggressive behaviors in AD are multicausal, with a greater weight of depressive and psychotic symptoms. Secondly, has observed that the appearance of aggressions increases as the disease worsens ,being less frequent at first. In terms of current treatments, the most effective ones are pharmacological, as well as new alternative therapies that are contributing to a better approach to symptoms. Following this line of research is really significant in order to be able to deal with aggressive behaviors of patients with AD in a more appropriate way and reduce the impact it has on patients, caregivers and family members

Additional file 1: Figure S1. of Slowly progressive dementia caused by MAPT R406W mutations: longitudinal report on a new kindred and systematic review

Additional neuropathology. Additional photomicrographs from three family members. Individuals, immunohistochemistry, and enlargement as indicated. (TIF 11179 kb

Additional file 1: Figure S1. of Slowly progressive dementia caused by MAPT R406W mutations: longitudinal report on a new kindred and systematic review

Additional neuropathology. Additional photomicrographs from three family members. Individuals, immunohistochemistry, and enlargement as indicated. (TIF 11179 kb