Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease?

Teipel, Stefan J.; Grothe, Michel J.

doi:10.1007/s00259-015-3222-3

Cited by 52 publications

(42 citation statements)

References 55 publications

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“…Therefore, our finding of significant MSE reduction in the rACC region in the LMCI group compared with the data in the NC group suggests that cognitive decline might be associated with disturbances of cognitive-emotional interactions in the brain. It has long been observed that progressive atrophy and glucose hypometabolism in the medial temporal lobe and cingulate cortex were associated with pre-symptomatic stages of AD (Fox et al, 2001;Knopman et al, 2013;Teipel et al, 2016). Together with the observations of a strong association of glucose metabolism with BOLD signals (Tomasi et al, 2013;Zhang et al, 2013), our evidence highlighted the involvement of rACC function in the neuropathology of cognitive decline in prodromal AD.…”

Section: Discussionsupporting

confidence: 76%

“…We anticipated lower MSE values in prodromal AD than in normal aging. Accumulating evidence indicates that the pathologies and functional abnormalities involved in the development of AD-associated cognitive deterioration are complex and vary by disease state (Lee et al, 2014;Teipel et al, 2016;Weiner et al, 2017;Fletcher et al, 2018). Therefore, in an effort to investigate pre-symptomatic AD progression at different stages, patients with MCI have been classified into two subgroups based upon clinical and behavioral measures provided by ADNI at the time of the imaging study: early MCI (EMCI) and late MCI (LMCI).…”

Section: Introductionmentioning

confidence: 99%

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Reduced Dynamic Complexity of BOLD Signals Differentiates Mild Cognitive Impairment From Normal Aging

Zheng

Onoda

Nagai

et al. 2020

Front. Aging Neurosci.

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Mild cognitive impairment (MCI) is characterized as a transitional phase between cognitive decline associated with normal aging and Alzheimer's disease (AD). Restingstate functional magnetic resonance imaging (fMRI) measuring blood oxygenation leveldependent (BOLD) signals provides complementary information considered essential for understanding disease progression. Previous studies suggested that multi-scale entropy (MSE) analysis quantifying the complexity of BOLD signals is a novel and promising method for investigating neurodegeneration associated with cognitive decline in different stages of MCI. Therefore, the current study used MSE to explore the changes in the complexity of resting-state brain BOLD signals in patients with early MCI (EMCI) and late MCI (LMCI). We recruited 345 participants' data from the Alzheimer's Disease Neuroimaging Initiative database, including 176 normal control (NC) subjects, 87 patients with EMCI and 82 patients with LMCI. We observed a significant reduction of brain signal complexity toward regularity in the left fusiform gyrus region in the EMCI group and in the rostral anterior cingulate cortex in the LMCI group. Our results extend prior work by revealing that significant reductions of brain BOLD signal complexity can be detected in different stages of MCI independent of age, sex and regional atrophy. Notably, the reduction of BOLD signal complexity in the rostral anterior cingulate cortex was significantly associated with greater risk of progression to AD. The present study thus identified MSE as a potential imaging biomarker for the early diagnosis of preclinical Alzheimer's disease and provides further insights into the neuropathology of cognitive decline in prodromal AD.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Reduced Dynamic Complexity of BOLD Signals Differentiates Mild Cognitive Impairment From Normal Aging

Zheng

Onoda

Nagai

et al. 2020

Front. Aging Neurosci.

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“…In recent work, AD pathology from preclinical to clinical stages was associated with decrease in the metabolism of the posterior cingulate cortex even before any sign of AD 34 . The appearance of hypometabolism prior to clinical change could vary depending on cognitive reserve.…”

Section: Discussionmentioning

confidence: 99%

Relationship betweenAPOEGenotype and Structural MRI Measures throughout Adulthood in the Study of Health in Pomerania Population-Based Cohort

Habes

Toledo

Resnick

et al. 2016

AJNR Am J Neuroradiol

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Background and Purpose The presence of the apolipoprotein E (APOE) ε4 allele is the strongest sporadic Alzheimer disease (AD) genetic risk factor. We hypothesized that APOE ε4 carriers and non-carriers may differ in imaging patterns already in the midlife. We therefore sought to identify the effect of APOE genotype on brain atrophy across almost the entire adult age span using advanced magnetic resonance imaging-based pattern analysis. Materials and Methods We analyzed MRI scans of 1,472 participants form the Study of Health in Pomerania (aged 22–90 years). We studied the association between age, APOE ε4 carrier status and brain atrophy, which was quantified using two magnetic resonance imaging-based indices: Spatial Pattern of Atrophy for Recognition of Brain Aging SPARE-BA (summarizing age-related brain atrophy) and SPARE-AD (summarizing AD-like brain atrophy patterns), as well as the gray matter volumes in several AD- and APOE-related regions of interest (lateral frontal, lateral temporal, medial frontal and hippocampus). Results No significant association was found between APOE ε4 carrier status and the studied regions of interest or the SPARE indices in linear regression models adjusted for age, gender, and education and including an interaction term between APOE and age. Conclusions Our study indicates that measurable APOE related brain atrophy does not occur in early adulthood and midlife and suggests that such atrophy may only occur more proximal to the onset of clinical symptoms of dementia.

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“…Moreover, connectivity has proved to be critical in the pathophysiology of the disease. Disconnection processes have been shown to be at least partly responsible for early hypometabolism in AD (Villain et al, 2010; Teipel and Grothe, 2016), and neuropathological research suggests that tau propagates transynaptically, neuron to neuron (Duyckaerts et al, 1997; Braak and Del Tredici, 2011; de Calignon et al, 2012; Ahmed et al, 2014). Finally, recent neuroimaging studies have shown that the topography of atrophy/hypometabolism in AD (and other forms of dementia) follows specific brain connectivity networks, as evidenced by resting-state functional magnetic resonance imaging (fMRI), for instance, leading to the network degeneration hypothesis (Seeley et al, 2009; La Joie et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Connectivity Disruption, Atrophy, and Hypometabolism within Posterior Cingulate Networks in Alzheimer's Disease

et al. 2016

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The posterior cingulate cortex (PCC) is a critical brain network hub particularly sensitive to Alzheimer's disease (AD) and can be subdivided into ventral (vPCC) and dorsal (dPCC) regions. The aim of the present study was to highlight functional connectivity (FC) disruption, atrophy, and hypometabolism within the ventral and dorsal PCC networks in patients with amnestic mild cognitive impairment (aMCI) or AD. Forty-three healthy elders (HE) (68.7 ± 6 years), 34 aMCI (73.4 ± 6.8 years) and 24 AD (70.9 ± 9.1 years) patients underwent resting-state functional MRI, anatomical T1-weighted MRI and FDG-PET scans. We compared FC maps obtained from the vPCC and dPCC seeds in HE to identify the ventral and dorsal PCC networks. We then compared patients and HE on FC, gray matter volume and metabolism within each network. In HE, the ventral PCC network involved the hippocampus and posterior occipitotemporal and temporoparietal regions, whereas the dorsal PCC network included mainly frontal, middle temporal and temporoparietal areas. aMCI patients had impaired ventral network FC in the bilateral hippocampus, but dorsal network FC was preserved. In AD, the ventral network FC disruption had spread to the left parahippocampal and angular regions, while the dorsal network FC was also affected in the right middle temporal cortex. The ventral network was atrophied in the bilateral hippocampus in aMCI patients, and in the vPCC and angular regions as well in AD patients. The dorsal network was only atrophied in AD patients, in the dPCC, bilateral supramarginal and temporal regions. By contrast, hypometabolism was already present in both the vPCC and dPCC networks in aMCI patients, and further extended to include the whole networks in AD patients. The vPCC and dPCC connectivity networks were differentially sensitive to AD. Atrophy and FC disruption were only present in the vPCC network in aMCI patients, and extended to the dPCC network in AD patients, suggesting that the pathology spreads from the vPCC to the dPCC networks. By contrast, hypometabolism seemed to follow a different route, as it was present in both networks since the aMCI stage, possibly reflecting not only local disruption but also distant synaptic dysfunction.

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Does posterior cingulate hypometabolism result from disconnection or local pathology across preclinical and clinical stages of Alzheimer’s disease?

Cited by 52 publications

References 55 publications

Reduced Dynamic Complexity of BOLD Signals Differentiates Mild Cognitive Impairment From Normal Aging

Reduced Dynamic Complexity of BOLD Signals Differentiates Mild Cognitive Impairment From Normal Aging

Relationship betweenAPOEGenotype and Structural MRI Measures throughout Adulthood in the Study of Health in Pomerania Population-Based Cohort

Connectivity Disruption, Atrophy, and Hypometabolism within Posterior Cingulate Networks in Alzheimer's Disease

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