Cognition, reserve, and amyloid deposition in normal aging

Rentz, Dorene M.; Locascio, Joseph J.; Becker, J. Alex; Moran, Erin K.; Eng, Elisha; Buckner, Randy L.; Sperling, Reisa A.; Johnson, Keith A.

doi:10.1002/ana.21904

Cited by 349 publications

(237 citation statements)

References 71 publications

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“…This [ 11 C]PIB accumulation seemed to reach a plateau at the level of dementia with moderate clinical severity (i.e., sum of the individual ratings of CDR Ͼ5) (Grimmer et al, 2009). In addition, recent studies also showed that [ 11 C]PIB uptake affected cognitive performance in normal aging Mormino et al, 2009;Rentz et al, 2010). These lines of evidence confirm that […”

Section: Similarity Index In Dmnsupporting

confidence: 69%

Effects of Brain Amyloid Deposition and Reduced Glucose Metabolism on the Default Mode of Brain Function in Normal Aging

Kikuchi¹,

Hirosawa²,

Yokokura³

et al. 2011

J. Neurosci.

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Brain ␤-amyloid (A␤) deposition during normal aging is highlighted as an initial pathogenetic event in the development of Alzheimer's disease. Many recent brain imaging studies have focused on areas deactivated during cognitive tasks [the default mode network (DMN), i.e., medial frontal gyrus/anterior cingulate cortex and precuneus/posterior cingulate cortex], where the strength of functional coordination was more or less affected by cerebral A␤ deposits. In the present positron emission tomography study, to investigate whether regional glucose metabolic alterations and A␤ deposits seen in nondemented elderly human subjects (n ϭ 22) are of pathophysiological importance in changes of brain hemodynamic coordination in DMN during normal aging, we measured cerebral glucose metabolism with [18 F]FDG, A␤ deposits with [ 11 C]PIB, and regional cerebral blood flow during control and working memory tasks by H 2 15 O on the same day. Data were analyzed using both region of interest and statistical parametric mapping. Our results indicated that the amount of A␤ deposits was negatively correlated with hemodynamic similarity between medial frontal and medial posterior regions, and the lower similarity was associated with poorer working memory performance. In contrast, brain glucose metabolism was not related to this medial hemodynamic similarity. These findings suggest that traceable A␤ deposition, but not glucose hypometabolism, in the brain plays an important role in occurrence of neuronal discoordination in DMN along with poor working memory in healthy elderly people.

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Section: Similarity Index In Dmnsupporting

confidence: 69%

Effects of Brain Amyloid Deposition and Reduced Glucose Metabolism on the Default Mode of Brain Function in Normal Aging

Kikuchi¹,

Hirosawa²,

Yokokura³

et al. 2011

J. Neurosci.

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“…[3][4][5][6] Studies using amyloid PET in cognitively normal elderly individuals and individuals with mild cognitive impairment (MCI) and AD dementia have found significant relationships between cognitive deficits and increased brain fibrillar amyloid using both cross-sectional [7][8][9][10][11][12] and longitudinal data [13][14][15][16][17][18][19][20][21][22][23] ; however, other studies have not shown amyloid and cognitive correlations. [24][25][26] In autosomal dominant AD (ADAD), brain amyloid deposition is known to occur 15 years or more before the onset of clinical symptoms, 27,28 and estimated years from expected symptom onset (EYO) calculated from family history data can provide an objective biomarkerindependent estimate of an individual's relative point in the disease process.…”

mentioning

confidence: 99%

Cerebral amyloidosis associated with cognitive decline in autosomal dominant Alzheimer disease

et al. 2015

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Objective: To investigate the associations of cerebral amyloidosis with concurrent cognitive performance and with longitudinal cognitive decline in asymptomatic and symptomatic stages of autosomal dominant Alzheimer disease (ADAD).Methods: Two hundred sixty-three participants enrolled in the Dominantly Inherited Alzheimer Network observational study underwent neuropsychological evaluation as well as PET scans with Pittsburgh compound B. One hundred twenty-one participants completed at least 1 follow-up neuropsychological evaluation. Four composite cognitive measures representing global cognition, episodic memory, language, and working memory were generated using z scores from a battery of 13 standard neuropsychological tests. General linear mixed-effects models were used to investigate the relationship between baseline cerebral amyloidosis and baseline cognitive performance and whether baseline cerebral amyloidosis predicts cognitive change over time (mean follow-up 2.32 years 6 0.92, range 0.89-4.19) after controlling for estimated years from expected symptom onset, APOE e4 allelic status, and education.Results: In asymptomatic mutation carriers, amyloid burden was not associated with baseline cognitive functioning but was significantly predictive of longitudinal decline in episodic memory. In symptomatic mutation carriers, cerebral amyloidosis was correlated with worse baseline performance in multiple cognitive composites and predicted greater decline over time in global cognition, working memory, and Mini-Mental State Examination.Conclusions: Cerebral amyloidosis predicts longitudinal episodic memory decline in presymptomatic ADAD and multidomain cognitive decline in symptomatic ADAD. These findings imply that amyloidosis in the brain is an indicator of early cognitive decline and provides a useful outcome measure for early assessment and prevention treatment trials. b-Amyloid (Ab) is thought to be an initiating factor in the pathophysiologic process of Alzheimer disease (AD).1,2 However, the relationship between cognition, brain Ab burden, and the future development of dementia is still unclear.

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“…5 The negative impact of neuropathology on cognition is weaker among higher reserve patients, as we have shown in MS 1,4 and others have shown in aging and Alzheimer disease. 6,7 In this context, the findings of Bonnet et al 2 conflict with the cognitive reserve literature, and therefore prompted this review of their study.…”

Section: Intellectual Enrichment Lessens the Effect Of Brain Atrophy mentioning

confidence: 98%

An unusual cause of isolated vomiting

Schlaeger

Sollberger²

2010

Neurology

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A 76-year-old woman with hypertension and diabetes presented with acute-onset vomiting. Her neurologic examination was unremarkable. When vomiting continued despite antiemetic therapy, brain MRI and magnetic resonance angiography were performed. These revealed an isolated region of restricted diffusion in the left area postrema (figure) together with basilar artery stenosis and filiform stenosis of the left vertebral artery.The rich vascularization of the area postrema, which is supplied from branches of the anterior cerebellar and the vertebral arteries, 1 may account for the lack of reported cases of infarctions of this medullary structure. While one small case series found that surgical ablation of the area postrema relieved patients of intractable vomiting, 2 our patient showed severe vomiting following infarction of only part of the area postrema. These contrasting findings imply that ischemia induced irritation, but not suppression, of the area postrema in our patient.

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Cognition, reserve, and amyloid deposition in normal aging

Cited by 349 publications

References 71 publications

Effects of Brain Amyloid Deposition and Reduced Glucose Metabolism on the Default Mode of Brain Function in Normal Aging

Effects of Brain Amyloid Deposition and Reduced Glucose Metabolism on the Default Mode of Brain Function in Normal Aging

Cerebral amyloidosis associated with cognitive decline in autosomal dominant Alzheimer disease

An unusual cause of isolated vomiting

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