Survival Profiles of Patients With Frontotemporal Dementia and Motor Neuron Disease

Hu, William T.; Seelaar, Harro; Josephs, Keith A.; Knopman, David S.; Boeve, Bradley F.; Sorenson, Eric J.; McCluskey, Leo; Elman, Lauren; Schelhaas, Helenius J.; Parisi, Joseph E.; Kuesters, Benno; Lee, Virginia M.‐Y.; Trojanowski, John Q.; Petersen, Ronald C.; Swieten, John van; Grossman, Murray

doi:10.1001/archneurol.2009.253

Cited by 86 publications

(65 citation statements)

References 27 publications

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“…However, some of the frailty components have been associated with survival in demented subjects. In fact, long-term survivors among demented subjects had delayed emergence of motor symptoms (Hu et al 2009), while unintentional weight loss was predictive of decreased survival in dementia (Aziz et al 2008). Physical activity can reduce the risk of cognitive decline and dementia (Fratiglioni and Wang 2007), but clinical trial evidence for the effectiveness of physical activity programs in managing or improving cognition, function, behavior, depression, and mortality in people with dementia is still insufficient overall (Forbes et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Frailty syndrome and all-cause mortality in demented patients: the Italian Longitudinal Study on Aging

Solfrizzi

Scafato

Frisardi

et al. 2011

AGE

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Cognition has already been considered as a component of frailty, and it has been demonstrated that it is associated with adverse health outcomes. We estimated the prevalence of frailty syndrome in an Italian older population and its predictive role on allcause mortality and disability in nondemented subjects and in demented patients. We evaluated 2,581 individuals recruited from the Italian Longitudinal Study on Aging, a population-based sample of 5,632 subjects, aged 65-84 years old. Participants received identical baseline evaluation at the 1st survey (1992)(1993) and were followed at 2nd (1995)(1996) and 3rd survey (2000)(2001). A phenotype of frailty according to partially modified measurement of Cardiovascular Health Study criteria was operationalized. The overall prevalence of frailty syndrome in this populationbased study was 7.6% (95% confidence interval (CI) 6.55-8.57). Frail individuals noncomorbid or nondisable were 9.1% and 39.3%, respectively, confirming an overlap but not concordance in the cooccurrence among these conditions. Frailty was associated with a significantly increased risk of allcause mortality over a 3-year follow-up (hazard ratio (HR) 1.98, 95% confidence interval (CI) 1.52-2.60) and over a 7-year follow-up (HR 1.74, 95% CI 1.44-2.16), but with significant increased risk of disability only over a 3-year follow-up (HR 1.32, 95% CI 1.06-1.86 over a 3-year follow-up and HR 1.16, 95% CI 0.88-1.56 over a 7-year follow-up). Frail demented patients were at higher risk of all-cause mortality over 3-(HR 3.33, 95% CI 1.28-8.29) and 7-year follow-up periods (HR 1.89, 95% CI 1.10-3.44), but not of disability. Frailty syndrome was a short-term predictor of disability in nondemented older subjects and short-and long-term predictor of all-cause mortality in nondemented and demented patients.

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Section: Discussionmentioning

confidence: 99%

Frailty syndrome and all-cause mortality in demented patients: the Italian Longitudinal Study on Aging

Solfrizzi

Scafato

Frisardi

et al. 2011

AGE

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“…There are various subtypes of PPA such as semantic dementia (svPPA), progressive non-fluent aphasia (nfvPPA), logopenic aphasia (LPA -an AD variant) and progressive apraxia of speech, based on speech pattern involved [99] . Pathologically, based on the protein involved, they are divided into the following three categories: (1) FTLD-tau: Including tauopathies such as progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), multisystem tauopathy with dementia and Pick's disease; (2) FTLD-TDP43: Transactive DNA-binding protein (TDP) 43 related abnormalities, a subgroup may also have motor neuron disease (MND) [100] ; and (3) FTLD-FUS: Fused in sarcoma (FUS) protein [101] .…”

Section: Frontotemporal Dementiamentioning

confidence: 99%

“…Various proteins including tauopathies, TDP43, FUSclinically can overlap with PSP, MSA, MND [100,101] Variable-predominantly anterior frontal, temporal and insular atrophy [102,103] FDG PET and SPECT-↓anterior, frontal and temporal uptake [107] fMRI, DTI-↓ in WM of affected regions [104] fMRI-↓"salient" network' but ↑DMN connectivity on resting fMRI-unlike AD [105,106] Vascular dementia…”

Section: Ftdmentioning

confidence: 99%

What can imaging tell us about cognitive impairment and dementia?

Narayanan

Murray

2016

WJR

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Dementia is a contemporary global health issue with far reaching consequences, not only for affected individuals and their families, but for national and global socioeconomic conditions. The hallmark feature of dementia is that of irreversible cognitive decline, usually affecting memory, and impaired activities of daily living. Advances in healthcare worldwide have facilitated longer life spans, increasing the risks of developing cognitive decline and dementia in late life. Dementia remains a clinical diagnosis. The role of structural and molecular neuroimaging in patients with dementia is primarily supportive role rather than diagnostic, American and European guidelines recommending imaging to exclude treatable causes of dementia, such as tumor, hydrocephalus or intracranial haemorrhage, but also to distinguish between different dementia subtypes, the commonest of which is Alzheimer's disease. However, this depends on the availability of these imaging techniques at individual centres. Advanced magnetic resonance imaging (MRI) techniques, such as functional connectivity MRI, diffusion tensor imaging and magnetic resonance spectroscopy, and molecular imaging techniques, such as 18F fluoro-deoxy glucose positron emission tomography (PET), amyloid PET, tau PET, are currently within the realm of dementia research but are available for clinical use. Increasingly the research focus is on earlier identification of at risk preclinical individuals, for example due to family history. Intervention at the preclinical stages before irreversible brain damage occurs is currently the best hope of reducing the impact of dementia.

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“…Este continuo clínico se ve reforzado a dos niveles: patológico, por la identificación de la proteína TDP43 (TAR DNA binding protein 43 kD) como el principal componente de las inclusiones ubiquitina positiva en ELA y en 50% de los casos con DFT 12,13 ; y a nivel genético por la identificación de la expansión de un hexanucleótido repetido en un intrón del gen C9ORF72 (cromosoma 9p21) en 25% de los casos con ELA familiar y 12% con DFT familiar 14,15 . Los pacientes con DFT que desarrollan ELA tienen una evolución más rápida y peor pronós-tico, pero no existen marcadores que permitan la realización de un diagnóstico precoz de DFT-ELA 9,16 . En este artículo revisamos la evidencia de la sobreposición entre DFT y ELA en cuanto al cuadro clínico y su relación con nuevos hallazgos genéticos y patológicos.…”

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Manifestaciones neuropsiquiátricas y cognitivas en demencia frontotemporal y esclerosis lateral amiotrófica: dos polos de una entidad común

et al. 2014

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Survival Profiles of Patients With Frontotemporal Dementia and Motor Neuron Disease

Cited by 86 publications

References 27 publications

Frailty syndrome and all-cause mortality in demented patients: the Italian Longitudinal Study on Aging

Frailty syndrome and all-cause mortality in demented patients: the Italian Longitudinal Study on Aging

What can imaging tell us about cognitive impairment and dementia?

Manifestaciones neuropsiquiátricas y cognitivas en demencia frontotemporal y esclerosis lateral amiotrófica: dos polos de una entidad común

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