"Frontotemporal dementia" from_date:2012

Automated free speech analysis reveals distinct markers of Alzheimer's and frontotemporal dementia. Dementia can disrupt how people experience and describe events as well as their own role in them. Alzheimer's disease (AD) compromises the processing of entities expressed by nouns, while behavioral variant frontotemporal dementia (bvFTD) entails a depersonalized perspective with increased third

Angioarchitectural alterations in the retina and choroid in frontotemporal dementia. Frontotemporal dementia (FTD) is a progressive neurodegenerative disorder that affects the frontal and temporal lobes of the brain, leading to cognitive decline and personality changes. The objective of this cross-sectional study was to characterize angioarchitectural changes in the retina and choroid

Intranasal oxytocin for apathy in people with frontotemporal dementia (FOXY): a multicentre, randomised, double-blind, placebo-controlled, adaptive, crossover, phase 2a/2b superiority trial. No treatments exist for apathy in people with frontotemporal dementia. Previously, in a randomised double-blind, placebo-controlled, dose-finding study, intranasal oxytocin administration in people with frontotemporal dementia improved apathy ratings on the Neuropsychiatric Inventory over 1 week and, in a randomised, double-blind, placebo-controlled, crossover study, a single dose of 72 IU oxytocin increased blood-oxygen-level-dependent signal in limbic brain regions. We aimed to determine whether longer treatment with oxytocin improves apathy in people with frontotemporal dementia. We conducted a multicentre

Altered spatiotemporal brain dynamics of interoception in behavioural-variant frontotemporal dementia. Dysfunctional allostatic-interoception, altered processing of bodily signals in response to environmental demands, occurs in behavioural-variant frontotemporal dementia (bvFTD) patients. Previous research has not investigated the dynamic nature of interoception using methods like intrinsic

Montreal Cognitive Assessment vs the Mini-Mental State Examination as a Screening Tool for Patients With Genetic Frontotemporal Dementia. With upcoming clinical trials targeting preclinical stages of genetic frontotemporal dementia (FTD), early detection through cognitive screening is crucial. The Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) have potential

Behavioural changes in frontotemporal dementia and their cognitive and neuroanatomical correlates. Behavioural changes are a central feature of frontotemporal dementia (FTD); they occur in both behavioural-variant (bvFTD) and semantic dementia (SD)/semantic-variant primary progressive aphasia subtypes. In this study, we addressed two current clinical knowledge gaps; (i) are there qualitative

Targeting nonsense-mediated RNA decay does not increase progranulin levels in the Grn R493X mouse model of frontotemporal dementia. A common cause of frontotemporal dementia (FTD) are nonsense mutations in the progranulin (GRN) gene. Because nonsense mutations activate the nonsense-mediated RNA decay (NMD) pathway, we sought to inhibit this RNA turnover pathway as a means to increase progranulin

Frontotemporal dementia Frontotemporal dementia - Symptoms, diagnosis and treatment | BMJ Best PracticeSkip to main contentSkip to search * About us * Help * Subscribe * Access through your institution * Log inBMJ Best Practice * Help * Getting started * FAQs * Contact us * Recent updates * Specialties * Calculators * Patient leaflets * Videos * Evidence * Drugs * Recent updates . The prevalence of frontotemporal dementia. Neurology. 2002 Jun 11;58(11):1615-21.http://www.ncbi.nlm.nih.gov/pubmed/12058088?tool=bestpractice.com[2]Rosso SM, Donker Kaat L, Baks T, et al. Frontotemporal dementia in the Netherlands: patient characteristics and prevalence estimates from a population-based study. Brain. 2003 Sep;126(Pt 9):2016-22.http://brain.oxfordjournals.org/content/126/9/2016.fullhttp

Longitudinal cerebral perfusion in presymptomatic genetic frontotemporal dementia: GENFI results. Effective longitudinal biomarkers that track disease progression are needed to characterize the presymptomatic phase of genetic frontotemporal dementia (FTD). We investigate the utility of cerebral perfusion as one such biomarker in presymptomatic FTD mutation carriers. We investigated longitudinal of hypoperfusion over time, with the left thalamus common to all groups. Frontal lobe regions featured lower perfusion in those who symptomatically converted versus asymptomatic carriers past their expected age of disease onset. Cerebral perfusion is a potential biomarker for assessing genetic FTD and its genetic subgroups prior to symptom onset. Gray matter perfusion declines in at-risk genetic frontotemporal

Clinical Accuracy of Serum Neurofilament Light to Differentiate Frontotemporal Dementia from Primary Psychiatric Disorders is Age-Dependent. Symptoms of behavioral variant frontotemporal dementia (bvFTD) overlap with primary psychiatric disorders (PPD) making diagnosis challenging. Serum neurofilament light (sNfL) is a candidate biomarker to distinguish bvFTD from PPD, but large-scale studies

Atrophy network mapping of clinical subtypes and main symptoms in frontotemporal dementia. Frontotemporal Dementia (FTD) is a disease of high heterogeneity, apathy and disinhibition present in all subtypes of FTD and imposes a significant burden on families/society. Traditional neuroimaging analysis has limitations in elucidating the network localization due to individual clinical

Data-driven analysis of regional brain metabolism in behavioral frontotemporal dementia and late-onset primary psychiatric diseases with frontal lobe syndrome: A PET/MRI study. Late-onset primary psychiatric disease (PPD) and behavioral frontotemporal dementia (bvFTD) present with a similar frontal lobe syndrome. We compare brain glucose metabolism in bvFTD and late-onset PPD and investigate

Resting-state alterations in behavioral variant frontotemporal dementia are related to the distribution of monoamine and GABA neurotransmitter systems. Aside to clinical changes, behavioral variant frontotemporal dementia (bvFTD) is characterized by progressive structural and functional alterations in frontal and temporal regions. We examined if there is a selective vulnerability of specific

Sleep and circadian rhythm disruptions in behavioral variant frontotemporal dementia. Sleep and rest-activity rhythm alterations are common in neurodegenerative diseases. However, their characterization in patients with behavioral variant frontotemporal dementia (bvFTD) has proven elusive. We investigated rest-activity rhythm alterations, sleep disturbances, and their neural correlates in bvFTD for ecologically monitoring changes in sleep duration in bvFTD patients. We assessed sleep and circadian rhythms in behavioral variant frontotemporal dementia (bvFTD) using actigraphy. Patients with bvFTD show increased sleep duration and reduced sleep quality. Patients with bvFTD show rest-activity alterations in the morning and early afternoon. Sleep duration is associated with reduced cortical thickness

Neuronal STING activation in amyotrophic lateral sclerosis and frontotemporal dementia. The stimulator of interferon genes (STING) pathway has been implicated in neurodegenerative diseases, including Parkinson's disease and amyotrophic lateral sclerosis (ALS). While prior studies have focused on STING within immune cells, little is known about STING within neurons. Here, we document neuronal ALS and frontotemporal dementia (FTD). To establish that STING activation occurs in a neuron-autonomous manner, we demonstrate the integrity of the STING signaling pathway, including both upstream activators and downstream innate immune response effectors, in dissociated mouse cortical neurons and neurons derived from control human induced pluripotent stem cells (iPSCs). Human iPSC-derived neurons

Genome-wide analyses reveal a potential role for the MAPT, MOBP, and APOE loci in sporadic frontotemporal dementia. Frontotemporal dementia (FTD) is the second most common cause of early-onset dementia after Alzheimer disease (AD). Efforts in the field mainly focus on familial forms of disease (fFTDs), while studies of the genetic etiology of sporadic FTD (sFTD) have been less common

Clinical recognition of frontotemporal dementia with right anterior temporal predominance: A multicenter retrospective cohort study. Although frontotemporal dementia (FTD) with right anterior temporal lobe (RATL) predominance has been recognized, a uniform description of the syndrome is still missing. This multicenter study aims to establish a cohesive clinical phenotype. Retrospective clinical

Beta-to-Theta Entropy Ratio of EEG in Aging, Frontotemporal Dementia, and Alzheimer's Dementia. Aging, frontotemporal dementia (FTD), and Alzheimer's dementia (AD) manifest electroencephalography (EEG) alterations, particularly in the beta-to-theta power ratio derived from linear power spectral density (PSD). Given the brain's nonlinear nature, the EEG nonlinear features could provide valuable

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia. Impaired social cognition is a core deficit in frontotemporal dementia (FTD). It is most commonly associated with the behavioural-variant of FTD, with atrophy of the orbitofrontal and ventromedial prefrontal cortex. Social cognitive changes are also common in semantic dementia, with atrophy centred

Synaptopathy: presynaptic convergence in frontotemporal dementia and amyotrophic lateral sclerosis. Frontotemporal dementia and amyotrophic lateral sclerosis are common forms of neurodegenerative disease which share overlapping genetics and pathologies. Crucially, no significantly disease-modifying treatments are available for either disease. Identifying the earliest changes which initiate neuronal dysfunction is important for designing effective intervention therapeutics. The genes mutated in genetic forms of frontotemporal dementia and amyotrophic lateral sclerosis have diverse cellular functions, and multiple disease mechanisms have been proposed for both. Identification of a convergent disease mechanism in frontotemporal dementia and amyotrophic lateral sclerosis would focus research