Investigation of frailty as a moderator of the relationship between neuropathology and dementia in Alzheimer's disease: a cross-sectional analysis of data from the Rush Memory and Aging Project

Wallace, Lindsay; Theou, Olga; Godin, Judith; Andrew, Melissa K.; Bennett, David A.; Rockwood, Kenneth

doi:10.1016/s1474-4422(18)30371-5

Cited by 237 publications

(212 citation statements)

References 30 publications

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“…Frailty is also associated with AD. 33 If this weight loss is linked to frailty, the weight loss may also impact survival. Further studies including food intake, energy expenditure, and frailty index are required to determine the mechanisms of weight loss in App NL-F/wt knock-in; ob/ob mice.…”

Section: Discussionmentioning

confidence: 99%

Increased levels of Aβ42 decrease the lifespan ofob/obmice with dysregulation of microglia and astrocytes

et al. 2019

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Abbreviations: Aβ, β-amyloid; AD, Alzheimer's disease; APP, amyloid precursor protein; CNS, central nervous system; DEA, diethylamine; GFAP, glial fibrillary acidic protein; INSR, insulin receptor; IRS1, insulin receptor substrate-1; IRS2, insulin receptor substrate-2; PDK1, pyruvate dehydrogenase kinase 1; PSD95, post-synaptic density protein 95; SYT1, synaptotagmin 1; NF-H, neurofilament heavy chain. AbstractClinical studies have indicated that obesity and diabetes are associated with Alzheimer's disease (AD) and neurodegeneration. Although the mechanisms underlying these associations remain elusive, the bidirectional interactions between obesity/ diabetes and Alzheimer's disease (AD) may be involved in them. Both obesity/ diabetes and AD significantly reduce life expectancy. We generated App NL-F/wt knock-in; ob/ob mice by crossing App NL-F/wt knock-in mice and ob/ob mice to investigate whether amyloid-β (Aβ) affects the lifespan of ob/ob mice. App NL-F/wt knock-in; ob/ob mice displayed the shortest lifespan compared to wild-type mice, App NL-F/wt knockin mice, and ob/ob mice. Notably, the Aβ42 levels were increased at minimum levels before deposition in App NL-F/wt knock-in mice and App NL-F/wt knock-in; ob/ob mice at 18 months of age. No differences in the levels of several neuronal markers were observed between mice at this age. However, we observed increased levels of glial fibrillary acidic protein (GFAP), an astrocyte marker, in App NL-F/wt knock-in; ob/ob mice, while the levels of several microglial markers, including CD11b, TREM2, and DAP12, were decreased in both ob/ob mice and App NL-F/wt knock-in; ob/ob mice. The increase in GFAP levels was not observed in young App NL-F/wt knock-in; ob/ob mice. |SHINOHARA et Al.

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Section: Discussionmentioning

confidence: 99%

Increased levels of Aβ42 decrease the lifespan ofob/obmice with dysregulation of microglia and astrocytes

et al. 2019

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“…As dementia prevention and fluid increasingly seems plausible, [92][93][94][95] CCCDTD has addressed risk reduction in this iteration. We took the approach that most dementia occurs in late life and typically has multiple causes 96,97 building on updates from a 2017 comprehensive overview of dementia prevention. 92 We supplemented information (when present) with updates, especially focusing on Canadian data.…”

Section: Risk Reductionmentioning

confidence: 99%

Recommendations of the 5th Canadian Consensus Conference on the diagnosis and treatment of dementia

Ismail

Black

Camicioli

et al. 2020

Alzheimer's & Dementia

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158

171

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Since 1989, four Canadian Consensus Conferences on the Diagnosis and Treatment of Dementia (CCCDTD) have provided evidence‐based dementia guidelines for Canadian clinicians and researchers. We present the results of the 5th CCCDTD, which convened in October 2019, to address topics chosen by the steering committee to reflect advances in the field, and build on previous guidelines. Topics included: (1) utility of the National Institute on Aging research framework for clinical Alzheimer's disease (AD) diagnosis; (2) updating diagnostic criteria for vascular cognitive impairment, and its management; (3) dementia case finding and detection; (4) neuroimaging and fluid biomarkers in diagnosis; (5) use of non‐cognitive markers of dementia for better dementia detection; (6) risk reduction/prevention; (7) psychosocial and non‐pharmacological interventions; and (8) deprescription of medications used to treat dementia. We hope the guidelines are useful for clinicians, researchers, policy makers, and the lay public, to inform a current and evidence‐based approach to dementia.

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“…This concept ties together two "giants of geriatrics", and may be a concept of interest for the future, especially in the studied population. A complex relationship between frailty and Alzheimer's dementia has very recently been described [170]. This work suggests that the degree of frailty may modify the association between cerebral Alzheimer's disease pathology and symptoms of Alzheimer's dementia.…”

Section: Clinical Considerationsmentioning

confidence: 81%

Geriatric Aspects of Frail Nursing Home Residents : A Swedish cohort study

Westerlind

2019

Linköping University Medical Dissertations

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Investigation of frailty as a moderator of the relationship between neuropathology and dementia in Alzheimer's disease: a cross-sectional analysis of data from the Rush Memory and Aging Project

Cited by 237 publications

References 30 publications

Increased levels of Aβ42 decrease the lifespan ofob/obmice with dysregulation of microglia and astrocytes

Increased levels of Aβ42 decrease the lifespan ofob/obmice with dysregulation of microglia and astrocytes

Recommendations of the 5th Canadian Consensus Conference on the diagnosis and treatment of dementia

Geriatric Aspects of Frail Nursing Home Residents : A Swedish cohort study

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