Glucose metabolism, gray matter structure, and memory decline in subjective memory impairment

Scheef, Lukas; Spottke, Annika; Daerr, Moritz; Joe, Alexius; Striepens, Nadine; Kölsch, Heike; Popp, Julius; Daamen, Marcel; Gorris, Dominik; Heneka, Michael T.; Boecker, Henning; Biersack, H. J.; Maier, Wolfgang; Schild, Hans H.; Wagner, Michael; Jessen, Frank

doi:10.1212/wnl.0b013e31826c1a8d

Cited by 253 publications

(216 citation statements)

References 38 publications

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“…Moreover, amyloid-positive subjects performed worse on SFN-N than those who were amyloid-negative. This is consistent with results reported by Rentz and coworkers (2011) in an English speaking population with the original FNAME test and using Pittsburgh compound B-positron emission tomography (PiB-PET) 11 . We used the Spanish version of FNAME (the S-FNAME) to determine whether it was also associated with Aβ burden in subjects with SCD as demonstrated with its original version (the FNAME) 15 .…”

Section: Discussionsupporting

confidence: 91%

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[O1–13–06]: The Spanish Version of Face‐name Associative Memory Exam (S‐fname) Performance Is Related to Amyloid Burden in Subjective Cognitive Decline

Alegret

Sanabria

Rodríguez-Gómez

et al. 2017

Alzheimer's & Dementia

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The Face-Name Associative Memory Exam (FNAME) is a paired associative memory test created to detect memory deficits in individuals with preclinical Alzheimer's disease (AD). Worse performance on FNAME in cognitively healthy individuals were found related to higher amyloid beta (Aβ) burden measured with Positron-Emission-Tomography using 11 C-PiB (PiB-PET). We previously reported normative data of a Spanish version of FNAME (S-FNAME) in cognitively healthy Spanish-speaking subjects. The aim of the present study was to determine whether performance on S-FNAME was associated with Aβ burden in subjective cognitive decline (SCD) individuals. 200 SCD subjects received neurological and neuropsychological assessments, including the S-FNAME and the Word List task from the Wechsler-Memory-Scale-III (WMS-III). Moreover, they received an MRI and (18)F-Florbetaben Positron-Emission-Tomography (FBB-PET) to measure Aβ burden. Three cognitive factor composites were derived for the episodic memory measures (face-name [SFN-N], face-occupation [SFN-O] and WMS-III) to determine whether episodic memory performance was related to Aβ deposition. Higher global Aβ deposition was significantly related to worse performance on SFN-N but not with SFN-O or WMS-III Composite. Moreover, worse SFN-N performance was significantly related to higher Aβ deposition in bilateral Posterior Cingulate Cortex. The S-FNAME may be a promising neuropsychological tool for detecting SCD individuals with preclinical AD.Alzheimer's disease (AD) is a major health problem with an estimated 50 million people worldwide living with dementia 1,2 with 33% of clinically normal older individuals having the underlying pathology of AD. With the advent of AD prevention trials, there is a growing interest in developing new diagnostic tools to detect the first symptoms of AD that may precede mild cognitive impairment (MCI).Subjective cognitive decline (SCD) has been proposed as a risk factor for progression to AD dementia 3,4 . It refers to the perception of memory or other cognitive problems without impairment on standardized cognitive tests. Longitudinal studies have demonstrated that cognitively healthy individuals with SCD have a [9][10][11][12] . Preclinical AD, by definition, is the identification of those clinically normal individuals with AD pathological burden. However, preclinical AD cannot be diagnosed with current standard neuropsychological tools and its diagnosis relies on the positivity of the different biomarkers of AD 13 . For this reason, there is an increasing interest in developing neuropsychological tools capable of identifying the subtle cognitive deficits present in the preclinical stage of AD 14 . The Face-Name Associative Memory Exam (FNAME), developed by Rentz and colleagues 15 , is a highly demanding face-name associative memory exam, but easy to administer and found useful for detecting evidence of amyloid-β (Aβ) burden related memory impairment in cognitively healthy individuals. The authors reported that lower performance on the FNAME were rela...

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Section: Discussionsupporting

confidence: 91%

“…It refers to the perception of memory or other cognitive problems without impairment on standardized cognitive tests. Longitudinal studies have demonstrated that cognitively healthy individuals with SCD have a [9][10][11][12] . Preclinical AD, by definition, is the identification of those clinically normal individuals with AD pathological burden.…”

mentioning

confidence: 99%

[O1–13–06]: The Spanish Version of Face‐name Associative Memory Exam (S‐fname) Performance Is Related to Amyloid Burden in Subjective Cognitive Decline

Alegret

Sanabria

Rodríguez-Gómez

et al. 2017

Alzheimer's & Dementia

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“…Even in some subjects with subjective memory impairment changes in metabolism have been observed, potentially reflecting early AD-typical pathological changes in the brain [258]. Interestingly, Reiman et al (1996) were able to demonstrate abnormalities even in APOE e4-positive subjects in younger age without any cognitive symptoms, underlining the high sensitivity of this method [259].…”

Section: Fluorodeoxyglucose-petmentioning

confidence: 81%

Perspective on future role of biological markers in clinical therapy trials of Alzheimer's disease: A long-range point of view beyond 2020

Hampel

Lista

Teipel

et al. 2014

Biochemical Pharmacology

105

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Recent advances in understanding the molecular mechanisms underlying various paths toward the pathogenesis of Alzheimer's disease (AD) has begun to provide new insight for interventions to modify disease progression. The evolving knowledge gained from multidisciplinary basic research has begun to identify new concepts for treatments and distinct classes of therapeutic targets; as well as putative disease-modifying compounds that are now being tested in clinical trials. There is a mounting consensus that such disease modifying compounds and/or interventions are more likely to be effectively administered as early as possible in the cascade of pathogenic processes preceding and underlying the clinical expression of AD. The budding sentiment is that "treatments" need to be applied before various molecular mechanisms converge into an irreversible pathway leading to morphological, metabolic and functional alterations that characterize the pathophysiology of AD. In light of this, biological indicators of pathophysiological mechanisms are desired to chart and detect AD throughout the asymptomatic early molecular stages into the prodromal and early dementia phase. A major conceptual development in the clinical AD research field was the recent proposal of new diagnostic criteria, which specifically incorporate the use of biomarkers as defining criteria for preclinical stages of AD. This paradigm shift in AD definition, conceptualization, operationalization, detection and diagnosis represents novel fundamental opportunities for the modification of interventional trial designs. This perspective summarizes not only present knowledge regarding biological markers but also unresolved questions on the status of surrogate indicators for detection of the disease in asymptomatic people and diagnosis of AD

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“…Whereas most studies have reported an association between SMCs and Ab, [3][4][5][6] others could not demonstrate this relationship. 7 Previous studies with fluorodeoxyglucose (FDG)-PET, a biomarker supposed to reflect neuronal integrity, 8 have demonstrated hypometabolism when comparing cognitively normal (CN) individuals with and without SMCs, but the results have been inconsistent as to which brain regions show hypometabolism, e.g., the precuneus, 9 parietotemporal and parahippocampal gyrus, 10 or periventricular region. 11 These inconsistent patterns of FDG-PET hypometabolism could be due to several factors, including the use of different techniques to measure SMCs.…”

mentioning

confidence: 99%

Hippocampal hypometabolism in older adults with memory complaints and increased amyloid burden

et al. 2017

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Objective: To identify the functional and pathologic correlates underlying subjective memory complaints (SMCs) in cognitively normal older adults.Methods: Two hundred fifty-one older adults underwent resting-state fluorodeoxyglucose (FDG)-PET and Pittsburg compound B-PET b-amyloid (Ab) imaging and filled out a questionnaire regarding SMCs. Participants were classified into 2 groups based on their Ab burden. Age-adjusted voxel-wise correlations were used to examine SMCs, amyloid status (Ab 1 vs Ab 2 ), and the interaction between SMCs and Ab status as predictors of metabolism. Region-of-interest (ROI) analyses were performed to confirm the whole-brain analyses and to test for additional covariates.Results: Greater SMCs correlated with decreased FDG metabolism in the bilateral precuneus, bilateral inferior parietal lobes, right inferior temporal lobe, right medial frontal gyrus, and right orbitofrontal gyrus. A significant interaction effect between SMCs and amyloid burden was found such that Ab 1 individuals with increased complaints had decreased FDG metabolism in the bilateral medial temporal lobes. ROI analyses confirmed the voxel-wise analyses result in that decreased precuneus metabolism was associated with greater SMCs regardless of Ab status, age, or thickness, whereas the relationship between hippocampal metabolism and SMCs was a function of Ab, even after adjustment for age, hippocampal volume, or depressive symptoms.Conclusions: These data show the relevant role of posterior and anterior midline regions in SMCs in older individuals. Decreased hippocampal metabolism may be a specific marker of subclinical changes in cognition due to amyloid pathology. However, longitudinal studies are needed to determine whether our findings foreshadow clinical decline. Neurology ® 2017;88:1759-1767 GLOSSARY Ab 5 b-amyloid; AD 5 Alzheimer disease; CN 5 cognitively normal; FDG 5 fluorodeoxyglucose; FDR 5 false discovery rate; GDS 5 Geriatric Depression Scale; MFG 5 middle frontal gyrus; MGH 5 Massachusetts General Hospital; MTL 5 medial temporal lobe; PiB 5 Pittsburg compound B; ROI 5 region of interest; SMC 5 subjective memory complaint.Subjective memory complaint (SMC) is defined by self-reports of memory worsening and objective memory performance in the normal adjusted range. SMCs are common in the elderly population without dementia, with an estimated prevalence range between 22% and 56%, 1 and have been associated with increased risk of incident Alzheimer disease (AD). 2 Despite the high prevalence of self-perceived changes in memory among older adults, relatively little is known about its functional and pathologic correlates, especially in the preclinical stages of AD. This information is crucial because SMCs alone may have insufficient sensitivity and specificity to predict the development of dementia.With regard to SMCs and b-amyloid (Ab; one hallmark of AD pathology most commonly used to define the preclinical stage), previous studies have found conflicting results. Whereas most studies have reported an a...

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Glucose metabolism, gray matter structure, and memory decline in subjective memory impairment

Cited by 253 publications

References 38 publications

[O1–13–06]: The Spanish Version of Face‐name Associative Memory Exam (S‐fname) Performance Is Related to Amyloid Burden in Subjective Cognitive Decline

[O1–13–06]: The Spanish Version of Face‐name Associative Memory Exam (S‐fname) Performance Is Related to Amyloid Burden in Subjective Cognitive Decline

Perspective on future role of biological markers in clinical therapy trials of Alzheimer's disease: A long-range point of view beyond 2020

Hippocampal hypometabolism in older adults with memory complaints and increased amyloid burden

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