Age-dependent accumulation of advanced glycosylation end products in human neurons

Li, Jenny J.; Surini, Maria; Catsicas, Stefan; Kawashima, Eric; Bouras, Constantin

doi:10.1016/0197-4580(95)80009-g

Cited by 61 publications

(32 citation statements)

References 34 publications

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“…Diabetic patients could have an increased risk of AD via AGE production since the modification of Aβ by AGE accelerates Aβ aggregation and the glycation of tau stabilizes neurofibrillary tangles [52]. High levels of AGE immunoreactivity are present in AD plaques and neurofibrillary tangles [89–92]. Moreover, RAGE has been found to be a receptor for Aβ and mediates Aβ induced microglia activation and subsequent inflammation in AD [93, 94].…”

Section: Oxidative Stress: Is It the Driving Force For Insulin Resmentioning

confidence: 99%

Elevated risk of type 2 diabetes for development of Alzheimer disease: A key role for oxidative stress in brain

Butterfield

Domenico

Barone

2014

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

322

244

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Alzheimer disease (AD) is the most common form of dementia among the elderly and is characterized by progressive loss of memory and cognition. Epidemiological data show that the incidence of AD increases with age and doubles every 5 years after 65 years of age. From a neuropathological point of view, amyloid-β-peptide (Aβ) leads to senile plaques, which, together with hyperphosphorylated tau-based neurofibrillary tangles and synapse loss, are the principal pathological hallmarks of AD. Aβ is associated with the formation of reactive oxygen (ROS) and nitrogen (RNS) species, and induces calcium-dependent excitotoxicity, impairment of cellular respiration, and alteration of synaptic functions associated with learning and memory. Oxidative stress was found to be associated with type 2 diabetes mellitus (T2DM), which (i) represents another prevalent disease associated with obesity and often aging, and (ii) is considered to be a risk factor for AD development. T2DM is characterized by high blood glucose levels resulting from increased hepatic glucose production, impaired insulin production and peripheral insulin resistance, which close resemble to the brain insulin resistance observed in AD patients. Furthermore, growing evidence suggest that oxidative stress play a pivotal role in the development of insulin resistance and vice versa. This review article provides molecular aspects and the pharmacological approaches from both preclinical and clinical data and interpreted from the point of view of oxidative stress with the aim to highlight progresses in this field.

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Section: Oxidative Stress: Is It the Driving Force For Insulin Resmentioning

confidence: 99%

Elevated risk of type 2 diabetes for development of Alzheimer disease: A key role for oxidative stress in brain

Butterfield

Domenico

Barone

2014

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

322

244

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“…Because these oxidation products tend to accumulate in the hippocampus during the course of normal ageing [44], and because they have also been associated with the senile plaques and neuro®brillary tangles that are characteristic of Alzheimer's disease (AD) [45], they are thought to play a role in the pathogenesis of neuronal damage in AD, although this hypothesis remains controversial [46,47]. Results from a large historical population cohort indicate that individuals with adultonset diabetes have a greatly increased risk of dementia, including AD [48], but clinical studies have typically failed to ®nd elevated rates of Type 2 diabetes in patients with AD [49], and autopsy studies have not detected more AD-type brain pathology (e.g.…”

Section: Hyperglycaemia-associated Pathophysiological Mechanismsmentioning

confidence: 99%

Why is learning and memory dysfunction in Type 2 diabetes limited to older adults?

Ryan

Geckle

2000

Diabetes Metab. Res. Rev.

166

119

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Review of the literature on the cognitive correlates and consequences of Type 2 diabetes reveals two very intriguing findings. Not only are verbal learning and memory skills most likely to be disrupted as compared to other cognitive skills (e.g. attention, executive function; psychomotor efficiency), but these mnestic deficits appear to be restricted to individuals with diabetes who are older than 60-65 years of age. Middle-aged adults with either Type 2 or Type 1 diabetes are apparently protected insofar as researchers have only infrequently reported learning and memory impairments in that age group. Why do older adults have such an increased risk of diabetes-associated memory dysfunction? In our view, this phenomenon is a consequence of a synergistic interaction between diabetes-related metabolic derangements and the structural and functional changes occurring in the central nervous system (CNS) that are part of the normal ageing process. To critically evaluate that possibility, we summarise what is known about learning and memory dysfunction in the adult with diabetes, examine the extent to which chronic hyperglycaemia may adversely affect the integrity of the CNS, and selectively review the literature on age-associated changes in brain morphology and cognitive function, paying special attention to the threshold theory of cognitive impairment.

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“…Normal aging human brain was shown to accumulate AGEs within neurons and glial cells [10,11] as well as in senile plaques [12]. Beside this "physiological" occurrence of AGEs, pathological accumulations of glycated proteins were found in neurodegenerative diseases such as Alzheimer's (AD) [13], Parkinson's [14], amyotrophic lateral sclerosis (ALS) [15,16], vascular dementia (VD) [17], CreutzfeldJakob (CJD) [18], Pick', and Lewy body diseases [7].…”

Section: Introductionmentioning

confidence: 99%

Characterization of the glycated human cerebrospinal fluid proteome

Ramírez-Boo¹,

Priego-Capote²,

Hainard³

et al. 2012

Journal of Proteomics

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Age-dependent accumulation of advanced glycosylation end products in human neurons

Cited by 61 publications

References 34 publications

Elevated risk of type 2 diabetes for development of Alzheimer disease: A key role for oxidative stress in brain

Elevated risk of type 2 diabetes for development of Alzheimer disease: A key role for oxidative stress in brain

Why is learning and memory dysfunction in Type 2 diabetes limited to older adults?

Characterization of the glycated human cerebrospinal fluid proteome

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