The significance of medial temporal lobe atrophy

Barkhof, Frederik; Polvikoski, Tuomo; Straaten, E.C.W. van; Kalaria, Raj N.; Sulkava, Raimo; Aronen, Hannu J.; Niinistö, Leena; Rastas, Sari; Oinas, Minna; Scheltens, Philip; Erkinjuntti, Timo

doi:10.1212/01.wnl.0000277459.83543.99

Cited by 183 publications

(125 citation statements)

References 27 publications

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“…We propose that the SNAP group could include 2 different subgroups: (1) patients with severe cortical damage and no hippocampal atrophy, who might have underlying frontotemporal degeneration or tangle-only dementia, and rapidly progress to dementia; and (2) patients with hippocampal atrophy but relatively preserved cortical metabolism, who might have either hippocampal sclerosis or argyrophilic grain disease. This hypothesis is in line with the observation that medial temporal lobe atrophy is related to primary degenerative hippocampal pathology in pathologically confirmed very old patients 24 who progress to dementia remarkably slowly. Current findings could have been influenced by the choice of biomarkers.…”

Section: Resultssupporting

confidence: 87%

Mild cognitive impairment with suspected nonamyloid pathology (SNAP)

et al. 2015

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Objectives: The aim of this study was to investigate predictors of progressive cognitive deterioration in patients with suspected non-Alzheimer disease pathology (SNAP) and mild cognitive impairment (MCI). Methods:We measured markers of amyloid pathology (CSF b-amyloid 42) and neurodegeneration (hippocampal volume on MRI and cortical metabolism on [18 F]-fluorodeoxyglucose-PET) in 201 patients with MCI clinically followed for up to 6 years to detect progressive cognitive deterioration. We categorized patients with MCI as A1/A2 and N1/N2 based on presence/absence of amyloid pathology and neurodegeneration. SNAPs were A2N1 cases.Results: The proportion of progressors was 11% (8/41), 34% (14/41), 56% (19/34), and 71%(60/85) in A2N2, A1N2, SNAP, and A1N1, respectively; the proportion of APOE e4 carriers was 29%, 70%, 31%, and 71%, respectively, with the SNAP group featuring a significantly different proportion than both A1N2 and A1N1 groups (p # 0.005). Hypometabolism in SNAP patients was comparable to A1N1 patients (p 5 0.154), while hippocampal atrophy was more severe in SNAP patients (p 5 0.002). Compared with A2N2, SNAP and A1N1 patients had significant risk of progressive cognitive deterioration (hazard ratio 5 2.7 and 3.8, p 5 0.016 and p , 0.001), while A1N2 patients did not (hazard ratio 5 1.13, p 5 0.771). In A1N2 and A1N1 groups, none of the biomarkers predicted time to progression. In the SNAP group, lower time to progression was correlated with greater hypometabolism (r 5 0.42, p 5 0.073). The amyloid cascade hypothesis 1,2 has so far dominated the Alzheimer disease (AD) field. Jack et al. Conclusions:3,4 proposed a dynamic model that relates disease stage to the best established biomarkers of AD pathology. Based on this, a National Institute on Aging-Alzheimer's Association task force developed recommendations for the diagnosis of preclinical AD based on biomarkers of amyloidosis and neuronal injury.5 Soon afterward, these criteria were operationalized and a

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Section: Resultssupporting

confidence: 87%

Mild cognitive impairment with suspected nonamyloid pathology (SNAP)

et al. 2015

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“…These data provide further evidence that hippocampal atrophy on MRI is a sensitive marker for ADrelated pathology, specifically for NFT-associated neurodegeneration. [7][8][9][10][11][12]29 An exception to this association is hippocampal-sparing atypical AD. 30,31 None of the patients in the current DLB cohort had the pathologic features of atypical hippocampal-sparing AD.…”

Section: Resultsmentioning

confidence: 99%

Focal atrophy on MRI and neuropathologic classification of dementia with Lewy bodies

Kantarci¹,

Ferman²,

Boeve³

et al. 2012

Neurology

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Objective: To determine the association between the focal atrophy measures on antemortem MRI and postmortem neuropathologic classification of dementia with Lewy bodies (DLB) using the Third Report of the DLB Consortium criteria. Methods:We retrospectively identified 56 subjects who underwent antemortem MRI and had Lewy body (LB) pathology at autopsy. Subjects were pathologically classified as high (n ϭ 25), intermediate (n ϭ 22), and low likelihood DLB (n ϭ 9) according to the Third Report of the DLB Consortium criteria. We included 2 additional pathologic comparison groups without LBs: one with low likelihood Alzheimer disease (AD) (control; n ϭ 27) and one with high likelihood AD (n ϭ 33). The associations between MRI-based volumetric measurements and the pathologic classification of DLB were tested with analysis of covariance by adjusting for age, sex, and MRI-to-death interval. Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia after Alzheimer disease (AD); however, many patients with DLB also have AD pathology. [1][2][3][4][5] Imaging markers that predict the contribution of AD to the dementia syndrome in DLB would have an important role in treatment decisions and assessing responsiveness to treatments targeting disease-specific pathologies. Results:According to the Third Report of the DLB Consortium criteria, 6 the pathologic diagnosis of DLB is made by considering both AD and Lewy body (LB) pathologies. For example, patients with limbic LBs are diagnosed as high likelihood DLB if they have low likelihood AD, but diagnosed as low likelihood DLB if they have high likelihood AD. Therefore, in vivo identification of AD and LB pathology is critical for the differential diagnosis of DLB.

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“…CT is also the most used brain imaging tool worldwide. Atrophy on CT 37 and MRI 23,38 have been related to neuropathologic findings. Fifth, multiple comparisons were made, which may lead to false-positive findings.…”

Section: Resultsmentioning

confidence: 99%