Longitudinal changes of cortical thickness in early- versus late-onset Alzheimer's disease

Cho, Hanna; Jeon, Sohee; Kang, Sohi; Lee, Jongmin; Lee, Jae Hong; Kim, Geon Ha; Shin, Jae Sung; Kim, Chi Hun; Noh, Young; Im, Kiho; Kim, Sung Tae; Chin, Juhee; Seo, Sang Won; Na, Duk L.

doi:10.1016/j.neurobiolaging.2013.01.004

Cited by 78 publications

(98 citation statements)

References 34 publications

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“…Slow progressors in our study were on average younger. Studies of imaging and pathology in AD show faster evolving brain atrophy in early-onset than in late-onset AD [28], which is in contrast to our study where some of the younger patients with mild or very mild AD showed little progression. The heterogeneity of our sample regarding age and disease severity indicates that age-related comorbidities may be of importance for disease progression although this could not be shown by the analyses in the present study [29].…”

Section: Discussioncontrasting

confidence: 99%

Progression of Alzheimer’s Disease: A Longitudinal Study in Norwegian Memory Clinics

Eldholm

Barca

Persson

et al. 2018

JAD

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Abstract.Background: The course of Alzheimer's disease (AD) varies considerably between individuals. There is limited evidence on factors important for disease progression. Objective: The primary aim was to study the progression of AD, as measured by the Clinical Dementia Rating Scale Sum of Boxes (CDR-SB). Secondary aims were to investigate whether baseline characteristics are important for differences in progression, and to examine the correlation between progression assessed using three different instruments: CDR-SB (0-18), the cognitive test Mini-Mental State Examination (MMSE, 0-30), and the functional measure Instrumental Activities of Daily Living (IADL, 0-1). Methods: The Progression of AD and Resource use (PADR) study is a longitudinal observational study in three Norwegian memory clinics. Results: In total, 282 AD patients (mean age 73.3 years, 54% female) were followed for mean 24 (16-37) months. The mean annual increase in CDR-SB was 1.6 (SD 1.8), the mean decrease in MMSE score 1.9 (SD 2.6), and the mean decrease in IADL score 0.13 (SD 0.14). Of the 282 patients, 132 (46.8%) progressed slowly, with less than 1 point yearly increase in CDR-SB. Cognitive test results at baseline predicted progression rate, and together with age, ApoE, history of hypertension, and drug use could explain 17% of the variance in progression rate. The strongest correlation of change was found between CDR-SB and IADL scores, the weakest between MMSE and IADL scores.

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Section: Discussioncontrasting

confidence: 99%

Progression of Alzheimer’s Disease: A Longitudinal Study in Norwegian Memory Clinics

Eldholm

Barca

Persson

et al. 2018

JAD

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“…Previous structural imaging studies have shown that greater cortical atrophy is present in EOAD, particularly in the parietal, dorsal temporal region, and the precuneus, whereas relatively greater medial temporal atrophy has been reported in LOAD. 11,29 These results suggest that the atrophy of limbic structures may be a prominent feature of LOAD but not of EOAD. 30,29 In line with these data, we hypothesized that the utility of the cortical sulcal markers in the diagnosis of AD would be higher in EOAD than in LOAD.…”

Section: Discussionmentioning

confidence: 78%

“…The involvement of the parietal areas in EOAD, especially the precuneus and the posterior cingulate, has been highlighted previously. 11,29,31 In contrast, the best marker for differentiating the LOAD patients from old controls remained images obtained from a single scanner improves diagnostic accuracy compared to using images acquired from multiple centers. 10,39 In the present study, we chose a methodological approach that avoids these issues.…”

Section: Discussionmentioning

confidence: 99%

“…More severe cortical atrophy in the temporo-parietal areas has been noted in EOAD, whereas greater medial temporal lobe atrophy has been observed in LOAD. 11 Cortical atrophy can be measured indirectly by measuring the sulcal width; such an approach is moving closer to clinical practice. Using three-dimensional image-processing techniques, [12][13][14] only few studies focusing on AD have found sulcal changes.…”

Section: Introductionmentioning

confidence: 99%

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Sulcal morphology as a new imaging marker for the diagnosis of early onset Alzheimer's disease

Hamelin

Bertoux

Bottlaender

et al. 2015

Neurobiology of Aging

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“…In fact, the early clinical symptoms in each variant correlate with functions subserved by the specifically involved networks (executive dysfunction in EOAD, language in lvPPA, and visual integration in PCA), rather than the commonly involved posterior DMN, suggesting that AD pathology in each variant may begin in the respective off-target network and later converge in the DMN. Although a small number of studies have investigated cognitive and structural changes over time in different AD variants (61)(62)(63)(64)(65), most of them included patients that were relatively advanced, providing limited information about the early stages of disease. However, it is also possible that the posterior DMN is less clinically eloquent than the off-target networks.…”

Section: Discussionmentioning

confidence: 99%

Intrinsic connectivity networks in healthy subjects explain clinical variability in Alzheimer’s disease

Lehmann

Madison

Ghosh

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

110

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Although previous studies have emphasized the vulnerability of the default mode network (DMN) in Alzheimer's disease (AD), little is known about the involvement of other functional networks and their relationship to clinical phenotype. To test whether clinicoanatomic heterogeneity in AD is driven by the involvement of specific networks, network connectivity was assessed in healthy subjects by seeding regions commonly and specifically atrophied in three clinical AD variants: early-onset AD (age at onset, <65 y; memory and executive deficits), logopenic variant primary progressive aphasia (language deficits), and posterior cortical atrophy (visuospatial deficits). Four-millimeter seed regions of interest were used to obtain intrinsic connectivity maps in 131 healthy controls (age, 65.5 ± 3.5 y). Atrophy patterns in independent cohorts of AD variant patients and their correspondence to connectivity networks in controls were also assessed. The connectivity maps of commonly atrophied regions of interest support posterior DMN and precuneus network involvement across AD variants, whereas seeding regions specifically atrophied in each AD variant revealed distinct, syndrome-specific connectivity patterns. Goodness-of-fit analysis of each connectivity map with network templates showed the highest correspondence between the early-onset AD seed connectivity map and anterior salience and right executive-control networks, the logopenic aphasia seed connectivity map and the language network, and the posterior cortical atrophy seed connectivity map and the higher visual network. Connectivity maps derived from controls matched regions commonly and specifically atrophied in the patients. Our findings indicate that the posterior DMN and precuneus network are commonly affected in AD variants, whereas syndrome-specific neurodegenerative patterns are driven by the involvement of specific networks outside the DMN. A lzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by extracellular accumulation of amyloid plaques, intracellular neurofibrillary tangles, and neuronal loss (1). Although most patients present with memory deficits, a significant minority of patients with AD present with nonamnestic syndromes (2, 3). Patients with nonfamilial early-onset AD (EOAD, defined as onset <65 y in most studies) often show heterogeneous cognitive deficits, including impairment in attention and executive functions (4, 5). Focal syndromes such as posterior cortical atrophy (PCA, characterized by predominant visuospatial and visuoperceptual deficits; ref. 6) and the logopenic variant of primary progressive aphasia [lvPPA, a progressive disorder of language (7,8)] are also most commonly caused by AD pathology. It has been suggested that up to 15% of patients with AD seen in dementia centers have nonamnestic presentations (2), and the importance of these syndromes is reflected in their inclusion in new diagnostic guidelines for AD (9, 10). The factors driving the clinicoanatomical heterogeneity in AD are not well understoo...

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Longitudinal changes of cortical thickness in early- versus late-onset Alzheimer's disease

Cited by 78 publications

References 34 publications

Progression of Alzheimer’s Disease: A Longitudinal Study in Norwegian Memory Clinics

Progression of Alzheimer’s Disease: A Longitudinal Study in Norwegian Memory Clinics

Sulcal morphology as a new imaging marker for the diagnosis of early onset Alzheimer's disease

Intrinsic connectivity networks in healthy subjects explain clinical variability in Alzheimer’s disease

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