Alzheimer's disease

Lane, Chris; Hardy, John; Schott, Jonathan M.

doi:10.1111/ene.13439

Cited by 1,969 publications

(1,566 citation statements)

References 73 publications

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“…Moreover, the question of whether (or when) neuroinflammation is protective, detrimental or perhaps both may well depend on disease stage and genotypes. Genetic factors, certain components of the innate immune system and vascular risk factors are likely to play a role in the pathogenesis of AD, but remains to be fully elucidated …”

Section: Discussionmentioning

confidence: 99%

Systemic inflammatory impact of periodontitis on cognitive impairment

et al. 2019

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Objectives The role in dementia of systemic inflammation derived from periodontal disease is not fully elucidated. The objective of our study was to examine the impact of inflammation on the relationship between periodontitis and cognitive impairment. Methods We have designed a case (n = 171) and control (n = 131) study to determine the periodontal health status, grade of cognitive impairment/dementia and systemic inflammation level, the last being measured by analysis of 29 inflammatory biomarkers using multiplex techniques. Results At the time of sampling, 11 of the 29 inflammatory biomarkers were associated with cognitive impairment in patients with more severe periodontitis. However, the inflammatory response to severe periodontitis was more reduced (lower biomarker concentrations) in cases (with cognitive impairment or dementia) than in (cognitively healthy) controls, an unexpected finding. Conclusions Based on these results, we cannot confirm that systemic inflammation derived from periodontal disease plays a relevant role in the aetiology of cognitive impairment.

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Section: Discussionmentioning

confidence: 99%

Systemic inflammatory impact of periodontitis on cognitive impairment

et al. 2019

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“…Alzheimer’s disease (AD) is a progressive neurodegenerative disease and the leading cause of dementia for the elderly population (Reitz & Mayeux, ). The cardinal hallmarks of AD mainly include amyloid beta senile plaques and neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau in the brain (Lane, Hardy, & Schott, ). Until now, the exact causal factors of AD remain not completely explored, while existing evidence suggest that dietary elements might be one of the key factors beneficially or adversely affecting AD progression (Dohrmann et al, ; Nakagawa et al, ; Perrone & Grant, ).…”

Section: Introductionmentioning

confidence: 99%

Quercetin is protective against short‐term dietary advanced glycation end products intake induced cognitive dysfunction in aged ICR mice

et al. 2020

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Dietary advanced glycation end products (dAGEs) might be potential toxins involved in the pathogenesis of Alzheimer’s disease (AD). Quercetin is a flavonoid possessing neuroprotective effects. We aimed to explore whether a 21 days of dAGEs intake would result in cognitive dysfunction in aged ICR mice, and the protective effects of quercetin, with potential mechanisms explored. Fourteen‐month old ICR mice were randomly assigned into four groups, that is, Control, AGEs, quercetin, and AGE diet supplemented with quercetin. Key markers involved in Aβ, tau, and neuroinflammation from hippocampus and cortex were measured via western blot. Gut microbiota and short chain fatty acids profiles from intestinal contents were measured via 16S rRNA gene sequencing and gas chromatography (GC), respectively. Quercetin alleviated cognitive impairment induced by dAGEs in aged mice. This might be associated with that quercetin reduced cathepsin B, tau phosphorylation, and neuroinflammation, and elevated α‐diversity index (ACE, Chao1, and Shannon index), and reduced phylum Verrucomicrobia of gut microbiota. Practical applications Alzheimer’s disease (AD) has been regarded as the commonest cause of progressive dementia for the elderly. This study is the very first to demonstrate that even a short‐term dietary advanced glycation end product (dAGEs) intake induced impaired cognitive function in aged ICR mice, and querectin is capable of reversing dAGEs‐induced cognitive dysfunction. Reduced tau phosphorylation, neuroinflammation, and altered gut microbiota profiles may be involved in querectin’s protective effects against dAGEs‐induced cognitive impairment. Our study suggested that quercetin supplementation might be beneficial for improving cognitive function in elderly subjects with high consumption of dAGEs such as grilling, frying, and broiling of food.

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“…Alzheimer's disease (AD) is still the principal concern all over the world regarding the ageing process, as it is the main cause of gradual enhancement in cognitive disability (Lane, Hardy, & Schott, ). It is well known that AD has a multifactorial aetiology resulting in progressive and irreversible dementia.…”

Section: Introductionmentioning

confidence: 99%

“…It is well known that AD has a multifactorial aetiology resulting in progressive and irreversible dementia. Most of the patients (99%) present the sporadic form of the disease, with a late onset (beginning after 65 years of age) characterized by an increase in amyloid‐β (Aβ) accumulation, leading to a great number of senile plaques, formation of neurofibrillary tangles, and inflammation (Ballard et al, ; Masters et al, ; Thal, Walter, Saido, & Fändrich, ; Scheltens et al, ; Lane et al, ). A small proportion of patients (1%), however, present the familial, most severe form of the disease, with mutations in genes related to the processing of Aβ peptide and early onset—around 45 years of age (Wattmo & Wallin, ).…”

Section: Introductionmentioning

confidence: 99%

α7 nicotinic ACh receptors are necessary for memory recovery and neuroprotection promoted by attention training in amyloid‐β‐infused mice

Telles-Longui

Mourelle

Schöwe

et al. 2019

British J Pharmacology

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Background and Purpose Attention training reverses the neurodegeneration and memory loss promoted by infusion of amyloid‐β (Aβ) peptide in rats and increases the density of α7 nicotinic ACh receptors (α7nAChRs) in brain areas related to memory. Hence, we aimed to assess the role of α7nAChRs in the memory recovery promoted by attention training. Experimental Approach C57Bl/6 mice were chronically infused with Aβ, Aβ plus the α7 antagonist methyllycaconitine (MLA), or MLA alone. Control animals were infused with vehicle. Animals were subjected weekly to the active avoidance shuttle box for 4 weeks (attention training). The brain and serum were collected for biochemical and histological analysis. Key Results Aβ caused cognitive impairment, which was reversed by the weekly training, whereas Aβ + MLA also promoted memory loss but with no reversal with weekly training. MLA alone also promoted memory loss but with only partial reversal with the training. Animals infused with Aβ alone showed senile plaques in hippocampus, no change in BDNF levels in cortex, hippocampus, and serum, but increased AChE activity in cortex and hippocampus. Co‐treatment with MLA increased AChE activity and senile plaque deposition in hippocampus as well as reducing BDNF in hippocampus and serum, suggesting a lack of α7nAChR function leads to a loss of neuroprotection mechanisms. Conclusions and Implications The α7nAChR has a determinant role in memory recovery and brain resilience in the presence of neurodegeneration promoted by Aβ peptide. These data support further studies concerning these receptors as pharmacological targets for future therapies.

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Alzheimer's disease

Cited by 1,969 publications

References 73 publications

Systemic inflammatory impact of periodontitis on cognitive impairment

Systemic inflammatory impact of periodontitis on cognitive impairment

Quercetin is protective against short‐term dietary advanced glycation end products intake induced cognitive dysfunction in aged ICR mice

α7 nicotinic ACh receptors are necessary for memory recovery and neuroprotection promoted by attention training in amyloid‐β‐infused mice

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