Metabolic-cognitive syndrome: A cross-talk between metabolic syndrome and Alzheimer's disease

Frisardi, Vincenza; Solfrizzi, Vincenzo; Seripa, Davide; Capurso, Cristiano; Santamato, Andrea; Sancarlo, Daniele; Vendemiale, Gianluigi; Pilotto, Alberto; Panza, Francesco

doi:10.1016/j.arr.2010.04.007

Cited by 288 publications

(197 citation statements)

References 223 publications

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“…10,11 Several possible mechanisms may explain an association between MetS and CI including microvascular and macrovascular disease, inflammation, adiposity, and insulin resistance. 12 Our study has some limitations, the most important the small sample size, but our results are consistent with a recent study that found an association between MetS, the number of its components and risk of developing CI in older women from clinical centers. 13 In fact, although the prevalence of MetS in our sample is not significantly different between people with Oral Communications DF, degree of freedom; n.s., not significant; BMI, body mass index; AO, abdominal obesity (defined by a waist circumference ≥102 cm for males and ≥88 cm for females); HTN, hypertension (BP>135/85 mmHg and/or antihypertensive drugs); BP, blood pressure; NIDDM, non insulin-dependent diabetes mellitus; TG, triglycerides; HTG, hypertriglyceridemia (TG>150 mg/dL and/or lipid-lowering drugs); TC, total cholesterol; HTC, hypercholesterolemia (TC≥240 mg/dL and/or lipid-lowering drugs); HDL-C, high density lipoprotein cholesterol (Low HDL-C when <40 mg/dL for males and <50 mg/dL for females); MetS, metabolic syndrome; NCEP ATPIII, National Cholesterol Education Program -Adult Treatment Panel III.…”

Section: Discussionsupporting

confidence: 82%

Metabolic syndrome and cognitive performance in the elderly

Rinaldi

Graffi²,

Gallone

et al. 2014

J Biol Res

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Metabolic syndrome (MetS) is a cluster of conditions, each of which represents a risk factor for cardiovascular disease: central obesity, hyperglycemia, dyslipidemia and hypertension. In different recent studies, MetS has been associated with an accelerate cognitive decline in the elderly. The aim of our research was to investigate the relationship between MetS and cognitive performance in 174 italian elderly people living in Val Cenischia (Piedmont, Italy). Mini mental state examination (MMSE) has been administered to assess the cognitive status of all participants. The prevalence of MetS is 50.3% (51.3 and 49.5% for males and females, respectively). Our results confirm the association between MetS and worse cognitive performance in the elderly: an increased number of MetS components is associated with an increased risk of developing cognitive impairment (odds ratio=1.54; confidence interval 95%:1.04-2.28; P<0.05).

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Section: Discussionsupporting

confidence: 82%

Metabolic syndrome and cognitive performance in the elderly

Rinaldi

Graffi²,

Gallone

et al. 2014

J Biol Res

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“…In support of this idea, various lifestyle‐related disorders, such as type II diabetes (T2DM), dyslipidemia, and obesity, have been epidemiologically linked to AD 2. Furthermore, AD and these metabolic disorders are commonly associated with a number of pathological features, including impairment of insulin signaling, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, oxidative stress, protein aggregation, and inflammation (Fig.…”

Section: Introductionmentioning

confidence: 99%

Importance of adiponectin activity in the pathogenesis of Alzheimer's disease

Waragai

Ho²,

Takamatsu

et al. 2017

Ann Clin Transl Neurol

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A recent study suggested that insulin resistance may play a central role in the pathogenesis of Alzheimer's disease (AD). In this regard, it is of note that upregulation of plasma adiponectin (APN), a benign adipokine that sensitizes the insulin receptor signaling pathway and suppresses inflammation, has recently been associated with the severities of amyloid deposits and cognitive deficits in the elderly, suggesting that APN may enhance the risk of AD. These results are unanticipated because AD has been linked to type II diabetes and other metabolic disorders in which hypoadiponectinemia has been firmly established, and because APN ameliorated neuropathological features in a mouse model of neurodegeneration. Therefore, the objective of this study is to discuss the possible mechanisms underlying the biological actions of APN in the context of AD. Given that insulin receptor signaling is required for normal function of the nervous system, we predict that APN may be upregulated to compensate for compromised activity of the insulin receptor signaling pathway. However, increased APN might be sequestered by tau in the brain, leading to neurotoxic protein aggregation in AD. Alternatively, misfolding of APN may result in downregulation of the insulin/APN signal transduction network, leading to decreased neuroprotective and neurotrophic activities. Thus, it is possible that both ‘gain of function’ and ‘loss of function’ of APN may underlie synaptic dysfunction and neuronal cell death in AD. Such a unique biological mechanism underlying APN function in AD may require a novel therapeutic strategy that is distinct from previous treatment for metabolic disorders.

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“…Metabolic syndrome, a condition characterized by multiple biochemical and physiological alterations like hyperglycemia, dyslipidemia, hypertension, obesity etc., has been linked with the genesis of sporadic AD [54]. Thus, there is substantial evidence supporting a strong metabolic component in AD pathogenesis which calls for a systematic discussion of metabolic risk factors of sporadic AD.…”

Section: Metabolic and Endocrine Components In Ad Pathogenesismentioning

confidence: 99%

Metabolic Risk Factors of Sporadic Alzheimer's Disease: Implications in the Pathology, Pathogenesis and Treatment

Chakrabarti¹,

Khemka²,

Banerjee³

et al. 2015

Aging and disease

105

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Alzheimer's disease (AD), the major cause of dementia among the elderly world-wide, manifests in familial and sporadic forms, and the latter variety accounts for the majority of the patients affected by this disease. The etiopathogenesis of sporadic AD is complex and uncertain. The autopsy studies of AD brain have provided limited understanding of the antemortem pathogenesis of the disease. Experimental AD research with transgenic animal or various cell based models has so far failed to explain the complex and varied spectrum of AD dementia. The review, therefore, emphasizes the importance of AD related risk factors, especially those with metabolic implications, identified from various epidemiological studies, in providing clues to the pathogenesis of this complex disorder. Several metabolic risk factors of AD like hypercholesterolemia, hyperhomocysteinemia and type 2 diabetes have been studied extensively both in epidemiology and experimental research, while much less is known about the role of adipokines, proinflammatory cytokines and vitamin D in this context. Moreover, the results from many of these studies have shown a degree of variability which has hindered our understanding of the role of AD related risk factors in the disease progression. The review also encompasses the recent recommendations regarding clinical and neuropathological diagnosis of AD and brings out the inherent uncertainty and ambiguity in this area which may have a distinct impact on the outcome of various population-based studies on AD-related risk factors.

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Metabolic-cognitive syndrome: A cross-talk between metabolic syndrome and Alzheimer's disease

Cited by 288 publications

References 223 publications

Metabolic syndrome and cognitive performance in the elderly

Metabolic syndrome and cognitive performance in the elderly

Importance of adiponectin activity in the pathogenesis of Alzheimer's disease

Metabolic Risk Factors of Sporadic Alzheimer's Disease: Implications in the Pathology, Pathogenesis and Treatment

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