β-Amyloid burden in healthy aging

Rodrigue, Karen M.; Kennedy, James L.; Devous, Michael D.; Rieck, Jenny; Hebrank, Andrew; Diaz‐Arrastia, Ramon; Mathews, Dana; Park, D. C.

doi:10.1212/wnl.0b013e318245d295

Cited by 349 publications

(340 citation statements)

References 38 publications

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“…Variability in the measurement of cognition is also large, ranging from tests developed for clinical use to experimental tests that may detect preclinical deficits. [11][12][13][14] Additionally, many studies have collapsed data across diagnostic groups, conflating diagnosis and cognitive status.…”

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confidence: 99%

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Meta-analysis of amyloid-cognition relations in cognitively normal older adults

et al. 2013

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Objective: We conducted a meta-analysis of relationships between amyloid burden and cognition in cognitively normal, older adult humans.Methods: Methods of assessing amyloid burden included were CSF or plasma assays, histopathology, and PET ligands. Cognitive domains examined were episodic memory, executive function, working memory, processing speed, visuospatial function, semantic memory, and global cognition. Sixty-four studies representing 7,140 subjects met selection criteria, with 3,495 subjects from 34 studies representing independent cohorts. Weighted effect sizes were obtained for each study. Primary analyses were conducted limiting to independent cohort studies using only the most common assessment method (Pittsburgh compound B). Exploratory analyses included all assessment methods.Results: Episodic memory (r 5 0.12) had a significant relationship to amyloid burden. Executive function and global cognition did not have significant relationships to amyloid in the primary analysis of Pittsburgh compound B (r 5 0.05 and r 5 0.08, respectively), but did when including all assessment methods (r 5 0.08 and r 5 0.09, respectively). The domains of working memory, processing speed, visuospatial function, and semantic memory did not have significant relationships to amyloid. Differences in the method of amyloid assessment, study design (longitudinal vs cross-sectional), or inclusion of control variables (age, etc.) had little influence.Conclusions: Based on this meta-analytic survey of the literature, increased amyloid burden has small but nontrivial associations with specific domains of cognitive performance in individuals who are currently cognitively normal. These associations may be useful for identifying preclinical Alzheimer disease or developing clinical outcome measures.

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confidence: 99%

“…The measures of global cognition in our analyses, with 1 exception, 14 included a submeasure of episodic memory. It is possible that memory provides an outsized contribution to the relation of global cognition and amyloid burden within cognitively normal adults.…”

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confidence: 99%

Meta-analysis of amyloid-cognition relations in cognitively normal older adults

et al. 2013

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“…Standard uptake value ratios (SUVRs) were computed for VOIs and a cerebellar VOI was extracted to determine nonspecific binding. As determined previously in healthy controls who underwent serial scanning performed by our research group and others, 24 a change in SUVRs greater than 8% per year was deemed to be a meaningful increase. All aspects of the study described herein were approved by the institutional review board at the University of Texas Southwestern Medical Center (Dallas, Texas) prior to the initiation of any study-specific procedures.…”

Section: Serial Florbetapir F18 Pet Imagingmentioning

confidence: 84%

Evidence of increased brain amyloid in severe TBI survivors at 1, 12, and 24 months after injury: report of 2 cases

Gatson

Stebbins²,

Mathews

et al. 2016

JNS

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Traumatic brain injury (TBI) is a major risk factor for Alzheimer’s disease. With respect to amyloid deposition, there are no published serial data regarding the deposition rate of amyloid throughout the brain after TBI. The authors conducted serial 18F-AV-45 (florbetapir F18) positron emission tomography (PET) imaging in 2 patients with severe TBI at 1, 12, and 24 months after injury. A total of 12 brain regions were surveyed for changes in amyloid levels. Case 1 involved a 50-year-old man who experienced a severe TBI. Compared with the 1-month time point, of the 12 brain regions that were surveyed, a decrease in amyloid (as indicated by standard uptake value ratios) was only observed in the hippocampus (−16%, left; −12%, right) and caudate nucleus (−18%, left; −18%, right), suggesting that initial amyloid accumulation in the brain was cleared between time points 1 and 12 months after injury. Compared to the scan at 1 year, a greater increase in amyloid (+15%) was observed in the right hippocampus at the 24-month time point. The patient in Case 2 was a 37-year-old man who suffered severe trauma to the head and a subsequent stroke; he had poor cognitive/functional outcomes and underwent 1.5 years of rehabilitation. Due to a large infarct area on the injured side of the brain (right side), the authors focused primarily on brain regions affected within the left hemisphere. Compared with the 1-month scan, they only found an increase in brain amyloid within the left anterior putamen (+11%) at 12 months after injury. In contrast, decreased amyloid burden was detected in the left caudate nucleus (−48%), occipital cortex (−21%), and precuneus (−19%) brain regions at the 12-month time point, which is indicative of early accumulation and subsequent clearance. In comparison with 12-month values, more clearance was observed, since a reduction in amyloid was found at 24 months after trauma within the left anterior putamen (−12%) and occipital cortex (−15%). Also, by 24 months, most of the amyloid had been cleared and the patient demonstrated improved results on the Rivermead symptom questionnaire, Glasgow Outcome Scale-Extended, and Disability Rating Scale. With respect to APOE status, the patient in Case 1 had two ε3 alleles and the patient in Case 2 had one ε2 and one ε3 allele. In comparison to the findings of the initial scan at 1 month after TBI, by 12 and 24 months after injury amyloid was cleared in some brain regions and increased in others. Serial imaging conducted here suggests that florbetapir F18 PET imaging may be useful in monitoring amyloid dynamics within specific brain regions following severe TBI and may be predictive of cognitive deficits.

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“…Ab accumulation in the brain reflects the onset of AD 31 . As taurine was reported to bind Ab peptides with weak anti-fibrillogenic effect, we measured alterations of plaque, soluble and insoluble forms of Ab 21,32 .…”

Section: Resultsmentioning

confidence: 99%

P4‐159: Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease

Kim

Yoon

et al. 2015

Alzheimer's & Dementia

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Alzheimer's disease (AD) is a lethal progressive neurological disorder affecting the memory. Recently, US Food and Drug Administration mitigated the standard for drug approval, allowing symptomatic drugs that only improve cognitive deficits to be allowed to accelerate on to clinical trials. Our study focuses on taurine, an endogenous amino acid found in high concentrations in humans. It has demonstrated neuroprotective properties against many forms of dementia. In this study, we assessed cognitively enhancing property of taurine in transgenic mouse model of AD. We orally administered taurine via drinking water to adult APP/ PS1 transgenic mouse model for 6 weeks. Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice. In the cortex of APP/PS1 mice, taurine slightly decreased insoluble fraction of Ab. While the exact mechanism of taurine in AD has not yet been ascertained, our results suggest that taurine can aid cognitive impairment and may inhibit Ab-related damages.

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β-Amyloid burden in healthy aging

Abstract: Even in a highly selected lifespan sample of adults, Aβ deposition is apparent in some adults and is influenced by APOE status. Greater amyloid burden was related to deleterious effects on cognition, suggesting that subtle cognitive changes accrue as amyloid progresses.

Cited by 349 publications

References 38 publications

Meta-analysis of amyloid-cognition relations in cognitively normal older adults

Meta-analysis of amyloid-cognition relations in cognitively normal older adults

Evidence of increased brain amyloid in severe TBI survivors at 1, 12, and 24 months after injury: report of 2 cases

P4‐159: Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease

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