Quantitative EEG Abnormalities and Cognitive Dysfunctions in Frontotemporal Dementia and Alzheimer’s Disease

2003 ◽  
Vol 15 (2) ◽  
pp. 106-114 ◽  
Author(s):  
M. Lindau ◽  
V. Jelic ◽  
S.-E. Johansson ◽  
C. Andersen ◽  
L.-O. Wahlund ◽  
...  
2011 ◽  
Vol 122 (9) ◽  
pp. 1718-1725 ◽  
Author(s):  
K. Nishida ◽  
M. Yoshimura ◽  
T. Isotani ◽  
T. Yoshida ◽  
Y. Kitaura ◽  
...  

2010 ◽  
Vol 121 ◽  
pp. S324
Author(s):  
K. Nishida ◽  
M. Yoshimura ◽  
Y. Kitaura ◽  
T. Isotani ◽  
T. Kinoshita

2021 ◽  
Vol 15 ◽  
Author(s):  
Nan Lin ◽  
Jing Gao ◽  
Chenhui Mao ◽  
Heyang Sun ◽  
Qiang Lu ◽  
...  

BackgroundAlzheimer’s disease (AD) and frontotemporal dementia (FTD) are the two main types of dementia. We investigated the electroencephalogram (EEG) difference and clinical correlation in early-onset Alzheimer’s disease (EOAD), and FTD using multimodal EEG analyses. EOAD had more severe EEG abnormalities than late-onset AD (LOAD). Group comparisons between EOAD and LOAD were also performed.MethodsThirty patients diagnosed with EOAD, nine patients with LOAD, and 14 patients with FTD (≤65 y) were recruited (2008.1–2020.2), along with 24 healthy controls (≤65 y, n = 18; >65 y, n = 6). Clinical data were reviewed. Visual EEG, EEG microstate, and spectral analyses were performed.ResultsCompared to controls, markedly increased mean microstate duration, reduced mean occurrence, and reduced global field power (GFP) peaks per second were observed in EOAD and FTD. We found increased durations of class B in EOAD and class A in FTD. EOAD had reduced occurrences in classes A, B, and C, while only class C occurrence was reduced in FTD. The visual EEG results did not differ between AD and FTD. Microstate B showed correlations with activities of daily living score (r = 0.780, p = 0.008) and cerebrospinal fluid (CSF) Aβ42 (r = −0.833, p = 0.010) in EOAD. Microstate D occurrence was correlated with the CSF Aβ42 level in FTD (r = 0.786, p = 0.021). Spectral analysis revealed a general slowing EEG, which may contribute to microstate dynamic loss. Power in delta was significantly higher in EOAD than in FTD all over the head. In addition, EOAD had a marked increased duration and decreased occurrence than late-onset AD (LOAD), with no group differences in visual EEG results.ConclusionThe current study found that EOAD and FTD had different EEG changes, and microstate had an association with clinical severity and CSF biomarkers. EEG microstate is more sensitive than visual EEG and may be useful for the differentiation between AD and FTD. The observations support that EEG can be a potential biomarker for the diagnosis and assessment of early-onset dementias.


2014 ◽  
Author(s):  
Joseph P. Barsuglia ◽  
Michelle J. Mather ◽  
Hemali V. Panchal ◽  
Aditi Joshi ◽  
Elvira Jimenez ◽  
...  

2020 ◽  
Vol 78 (2) ◽  
pp. 537-541
Author(s):  
Jordi A. Matias-Guiu ◽  
Vanesa Pytel ◽  
Jorge Matías-Guiu

We aimed to evaluate the frequency and mortality of COVID-19 in patients with Alzheimer’s disease (AD) and frontotemporal dementia (FTD). We conducted an observational case series. We enrolled 204 patients, 15.2% of whom were diagnosed with COVID-19, and 41.9% of patients with the infection died. Patients with AD were older than patients with FTD (80.36±8.77 versus 72.00±8.35 years old) and had a higher prevalence of arterial hypertension (55.8% versus 26.3%). COVID-19 occurred in 7.3% of patients living at home, but 72.0% of those living at care homes. Living in care facilities and diagnosis of AD were independently associated with a higher probability of death. We found that living in care homes is the most relevant factor for an increased risk of COVID-19 infection and death, with AD patients exhibiting a higher risk than those with FTD.


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Adeline Su Lyn Ng ◽  
Juan Wang ◽  
Kwun Kei Ng ◽  
Joanna Su Xian Chong ◽  
Xing Qian ◽  
...  

Abstract Background Alzheimer’s disease (AD) and behavioral variant frontotemporal dementia (bvFTD) cause distinct atrophy and functional disruptions within two major intrinsic brain networks, namely the default network and the salience network, respectively. It remains unclear if inter-network relationships and whole-brain network topology are also altered and underpin cognitive and social–emotional functional deficits. Methods In total, 111 participants (50 AD, 14 bvFTD, and 47 age- and gender-matched healthy controls) underwent resting-state functional magnetic resonance imaging (fMRI) and neuropsychological assessments. Functional connectivity was derived among 144 brain regions of interest. Graph theoretical analysis was applied to characterize network integration, segregation, and module distinctiveness (degree centrality, nodal efficiency, within-module degree, and participation coefficient) in AD, bvFTD, and healthy participants. Group differences in graph theoretical measures and empirically derived network community structures, as well as the associations between these indices and cognitive performance and neuropsychiatric symptoms, were subject to general linear models, with age, gender, education, motion, and scanner type controlled. Results Our results suggested that AD had lower integration in the default and control networks, while bvFTD exhibited disrupted integration in the salience network. Interestingly, AD and bvFTD had the highest and lowest degree of integration in the thalamus, respectively. Such divergence in topological aberration was recapitulated in network segregation and module distinctiveness loss, with AD showing poorer modular structure between the default and control networks, and bvFTD having more fragmented modules in the salience network and subcortical regions. Importantly, aberrations in network topology were related to worse attention deficits and greater severity in neuropsychiatric symptoms across syndromes. Conclusions Our findings underscore the reciprocal relationships between the default, control, and salience networks that may account for the cognitive decline and neuropsychiatric symptoms in dementia.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Patricia Yuste-Checa ◽  
Victoria A. Trinkaus ◽  
Irene Riera-Tur ◽  
Rahmi Imamoglu ◽  
Theresa F. Schaller ◽  
...  

AbstractSpreading of aggregate pathology across brain regions acts as a driver of disease progression in Tau-related neurodegeneration, including Alzheimer’s disease (AD) and frontotemporal dementia. Aggregate seeds released from affected cells are internalized by naïve cells and induce the prion-like templating of soluble Tau into neurotoxic aggregates. Here we show in a cellular model system and in neurons that Clusterin, an abundant extracellular chaperone, strongly enhances Tau aggregate seeding. Upon interaction with Tau aggregates, Clusterin stabilizes highly potent, soluble seed species. Tau/Clusterin complexes enter recipient cells via endocytosis and compromise the endolysosomal compartment, allowing transfer to the cytosol where they propagate aggregation of endogenous Tau. Thus, upregulation of Clusterin, as observed in AD patients, may enhance Tau seeding and possibly accelerate the spreading of Tau pathology.


2017 ◽  
Vol 33 (1) ◽  
pp. 141-150 ◽  
Author(s):  
Marta Fernández-Matarrubia ◽  
Jordi A. Matías-Guiu ◽  
María Nieves Cabrera-Martín ◽  
Teresa Moreno-Ramos ◽  
María Valles-Salgado ◽  
...  

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