Apathy Is Associated With Increased Amyloid Burden in Mild Cognitive Impairment

Marshall, Gad A.; Donovan, Nancy J.; Lorius, Natacha; Gidicsin, Christopher; Maye, Jacqueline; Pepin, Lesley; Becker, J. Alex; Amariglio, Rebecca E.; Rentz, Dorene M.; Sperling, Reisa A.; Johnson, Keith A.

doi:10.1176/appi.neuropsych.12060156

Cited by 57 publications

(46 citation statements)

References 44 publications

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“…Subjects with depressive symptoms often suffer from additional neuropsychiatric symptoms such as anxiety or apathy [40, 41] which may be independent factors contributing to amyloid or metabolism status. However, had we restricted our search to patients positive for depressive symptoms only, the group size would have been too low to allow statistical comparison.…”

Section: Discussionmentioning

confidence: 99%

Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients

Brendel¹,

Pogarell

Xiong

et al. 2015

Eur J Nucl Med Mol Imaging

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Purpose Late-life depression (LLD) even in subsyndromal stages revealed strong associations with Alzheimer’s disease (AD). Furthermore brain amyloidosis depicts an early biomarker in subjects subsequently suffering from AD and is sensitively detectable by amyloid-PET. Therefore we aimed to compare amyloid-load and glucose metabolism in subsyndromally depressed mild cognitive impaired (MCI) subjects. Methods 371 MCI subjects from ADNI underwent [18F]-AV45-, [18F]-FDG-PET, and MRI. Subjects were judged β-amyloid positive (Aß(+); N=206) or negative (Aß(−); N=165) according to [18F]-AV45-PET. Depressive symptoms were assessed by the Neuropsychiatric Inventory Questionnaire (NPI-Q) depression-item. 65 Aß(+) and 41 Aß(−) subjects with depressive symptoms (DEP) were contrasted against their non-depressed (NON-DEP) counterparts. Conversion rates to AD were analysed (mean follow-up time: 21.5±9.1 months) with regard to coexisting depressive symptoms and brain amyloid-load. Results Aß(+) DEP subjects showed large clusters with higher amyloid-load in frontotemporal and insular cortices (p<0.001) and coincident hypermetabolism (p<0.001) in frontal cortices when contrasted against NON-DEP. Faster progression to AD was observed in subjects with either depressive symptoms (p<0.005) or Aß(+) status (p<0.001). Coincident depressive symptoms additionally shortened the conversion time in all Aß(+) subjects (p<0.005) and to a greater extent in a subgroup with high amyloid-load (p<0.001). Conclusions Our results clearly indicate that Aß(+) MCI subjects with depressive symptoms suffer from elevated amyloid-load combined with relative hypermetabolism of connected brain areas when contrasted against cognitively-matched non-depressed individuals. MCI subjects with high amyloid-load and coexistent depressive symptoms represent a high-risk group for faster conversion to AD.

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Section: Discussionmentioning

confidence: 99%

Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients

Brendel¹,

Pogarell

Xiong

et al. 2015

Eur J Nucl Med Mol Imaging

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“…Associations between apathy and atrophy of the medial frontal regions have also been found in related neurodegenerative dementias {37}. Moreover, associations between apathy and cortical amyloid burden have been detected as early as MCI {13}. Since cortical thinning patterns associated with AD have been detected as early as the preclinical stages of AD in PiB-positive CN individuals {11, 38}, it is plausible to hypothesize that apathy-associated patterns of atrophy may begin at the stage of MCI or earlier.…”

Section: Discussionmentioning

confidence: 99%

“…Cortical thinning has been detected in clinically normal (CN) elderly individuals with greater amyloid burden seen on Pittsburgh Compound B (PiB) positron emission tomography (PET) {11, 12} and apathy has been associated with increased cortical amyloid burden in MCI {13}. Accordingly, cortical thinning has been detected in CN individuals with low cerebrospinal fluid amyloid-β 1–42 {14}.…”

Section: Introductionmentioning

confidence: 99%

Apathy is Associated With Lower Inferior Temporal Cortical Thickness in Mild Cognitive Impairment and Normal Elderly Individuals

Guercio¹,

Donovan²,

Ward³

et al. 2015

JNP

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Apathy is a common neuropsychiatric symptom in Alzheimer’s disease (AD) dementia and amnestic mild cognitive impairment (MCI) and is associated with cortical atrophy in AD dementia. This study investigated possible correlations between apathy and cortical atrophy in 47 individuals with MCI and 19 clinically normal elderly (CN). Backward elimination multivariate linear regression was used to evaluate the cross-sectional relationship between scores on the Apathy Evaluation Scale and thickness of several cortical regions and covariates. Lower inferior temporal cortical thickness was predictive of greater apathy. Greater anterior cingulate cortical thickness was also predictive of greater apathy, suggesting an underlying reactive process.

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“…A significant association was found between increased apathy (a lower Apathy Evaluation Scale score) and greater cortical PiB retention independent of age, but no significant association between apathy and regional fluorodeoxyglucose (FDG) metabolism. 21 Also, elevated CSF tau was found to be associated with psychosis in AD. 22 Routine laboratory exams.…”

Section: Diagnosis Of Cognitive Decline In Futurementioning

confidence: 99%

Clinical workout for the early detection of cognitive decline and dementia

Tsolaki

2014

Eur J Clin Nutr

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Aging is the major risk factor for the development of human neurodegenerative maladies such as Alzheimer's, Huntington's and Parkinson's diseases (PDs) and prion disorders, all of which stem from toxic protein aggregation. All of these diseases are correlated with cognitive decline. Cognitive Decline is a dynamic state from normal cognition of aging to dementia. According to the original criteria for Alzheimer's Disease (AD) (1984), a clinical diagnosis was possible only when someone was already demented. The prevalence rates of Cognitive Decline (mild cognitive impairment plus dementia) are very high now and will be higher in future because of the increasing survival time of people. Many neurological and psychiatric diseases are correlated with cognitive decline. Diagnosis of cognitive decline is mostly clinical (clinical criteria), but there are multiple biomarkers that could help us mostly in research programs such as short or long, paper and pencil or computerized neuropsychological batteries for cognition, activities of daily living and behavior, electroencephalograph, event-related potentials, and imaging-structural magnetic resonance imaging (MRI) and functional (fMRI, Pittsburgh bound positron emission tomography, FDG-PET, single photon emission computerized tomography and imaging of tau pathology)-cerebrospinal fluid proteins (Abeta, tau and phospho-tau in AD and α-synuclein (αSyn) for PD). Blood biomarkers need more studies to confirm their usefulness. Genetic markers are also studied but until now are not used in clinical praxis. Finally, in everyday clinical praxis and in research workout for early detection of cognitive decline, the combination of biomarkers is useful.

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Apathy Is Associated With Increased Amyloid Burden in Mild Cognitive Impairment

Cited by 57 publications

References 44 publications

Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients

Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients

Apathy is Associated With Lower Inferior Temporal Cortical Thickness in Mild Cognitive Impairment and Normal Elderly Individuals

Clinical workout for the early detection of cognitive decline and dementia

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