Brain

Berti, Valentina; Mosconi, Lisa; Pupi, Alberto

doi:10.1016/j.cpet.2013.10.006

Cited by 102 publications

(28 citation statements)

References 64 publications

(63 reference statements)

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“…Positron emission tomography (PET) studies with 18 F-fluorodeoxy-2-glucose (FDG) as the tracer has consistently documented that reduction in brain CMRglc develop years, if not decades, prior to onset of clinical symptoms [ 12 – 16 ], correlate with AD progression [ 17 ], and are more severe in women than in men [ 18 ]. Glucose dysmetabolism in AD occurs in conjunction with mitochondrial dysfunction, particularly reduced COX activity in brain tissue, fibroblasts and platelets in humans, and is extensively documented in preclinical models of prodromal AD [ 11 , 19 – 21 ].…”

Section: Introductionmentioning

confidence: 99%

Perimenopause and emergence of an Alzheimer’s bioenergetic phenotype in brain and periphery

et al. 2017

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After advanced age, female sex is the major risk factor for Alzheimer’s disease (AD). The biological mechanisms underlying the increased AD risk in women remain largely undetermined. Preclinical studies identified the perimenopause to menopause transition, a neuroendocrine transition state unique to the female, as a sex-specific risk factor for AD. In animals, estrogenic regulation of cerebral glucose metabolism (CMRglc) falters during perimenopause. This is evident in glucose hypometabolism and decline in mitochondrial efficiency which is sustained thereafter. This study bridges basic to clinical science to characterize brain bioenergetics in a cohort of forty-three, 40–60 year-old clinically and cognitively normal women at different endocrine transition stages including premenopause (controls, CNT, n = 15), perimenopause (PERI, n = 14) and postmenopause (MENO, n = 14). All participants received clinical, laboratory and neuropsychological examinations, 18F-fluoro-deoxyglucose (FDG)-Positron Emission Tomography (PET) FDG-PET scans to estimate CMRglc, and platelet mitochondrial cytochrome oxidase (COX) activity measures. Statistical parametric mapping and multiple regression models were used to examine clinical, CMRglc and COX data across groups. As expected, the MENO group was older than PERI and controls. Groups were otherwise comparable for clinical measures and distribution of APOE4 genotype. Both MENO and PERI groups exhibited reduced CMRglc in AD-vulnerable regions which was correlated with decline in mitochondrial COX activity compared to CNT (p’s<0.001). A gradient in biomarker abnormalities was most pronounced in MENO, intermediate in PERI, and lowest in CNT (p<0.001). Biomarkers correlated with immediate and delayed memory scores (Pearson’s 0.26≤r≤0.32, p≤0.05). These findings validate earlier preclinical findings and indicate emergence of bioenergetic deficits in perimenopausal and postmenopausal women, suggesting that the optimal window of opportunity for therapeutic intervention in women is early in the endocrine aging process.

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Section: Introductionmentioning

confidence: 99%

Perimenopause and emergence of an Alzheimer’s bioenergetic phenotype in brain and periphery

et al. 2017

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“…Notably, many noncancerous tissues, including the brain, are FDG-PET avid (Berti et al, 2014; Cohade, 2010), illustrating that high glucose uptake is not a unique feature of tumors and offering a potential explanation for the relative lack of success in directly targeting glucose metabolism for cancer treatment. Doses of 2-DG that inhibit glycolysis enough to limit cancer growth may not be tolerated due to similar effects in normal tissues that also rely on glucose metabolism.…”

Section: Altered Glucose Metabolismmentioning

confidence: 99%

Targeting Metabolism for Cancer Therapy

Luengo

Gui

Heiden

2017

Cell Chemical Biology

733

624

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Metabolic reprogramming contributes to tumor development and introduces metabolic liabilities that can be exploited to treat cancer. Chemotherapies targeting metabolism have been effective cancer treatments for decades, and the success of these therapies demonstrates that a therapeutic window exists to target malignant metabolism. New insights into the differential metabolic dependencies of tumors have provided novel therapeutic strategies to exploit altered metabolism, some of which are being evaluated in pre-clinical models or clinical trials. Here, we review our current understanding of cancer metabolism and discuss how this might guide treatments targeting the metabolic requirements of tumor cells.

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“…According to several studies, the deregulation of glucose metabolism in AD can be controlled by the administration of a hormone known as a potent regulator of glucose homeostasis [ 11 ] and of food intake [ 12 ], glucagon-like peptide 1 (GLP-1) [ 13 ]. The fact that administration of this peptide improves cognitive decline in patients with AD, as well as in AD mouse model [ 14 , 15 ] suggests that deregulation of glucose in the brain is a crucial issue in the onset and progression of AD [ 4 , 5 , 16 , 17 , 18 ]. Here, we review recent evidence concerning the role of GLP-1 in diabetes-induced dementia.…”

Section: Introductionmentioning

confidence: 99%

The Role of Glucagon-Like Peptide 1 (GLP1) in Type 3 Diabetes: GLP-1 Controls Insulin Resistance, Neuroinflammation and Neurogenesis in the Brain

Bae

Song

2017

IJMS

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Alzheimer’s disease (AD), characterized by the aggregation of amyloid-β (Aβ) protein and neuroinflammation, is the most common neurodegenerative disease globally. Previous studies have reported that some AD patients show impaired glucose utilization in brain, leading to cognitive decline. Recently, diabetes-induced dementia has been called “type 3 diabetes”, based on features in common with those of type 2 diabetes and the progression of AD. Impaired glucose uptake and insulin resistance in the brain are important issues in type 3 diabetes, because these problems ultimately aggravate memory dysfunction in the brain. Glucagon-like peptide 1 (GLP-1) has been known to act as a critical controller of the glucose metabolism. Several studies have demonstrated that GLP-1 alleviates learning and memory dysfunction by enhancing the regulation of glucose in the AD brain. However, the specific actions of GLP-1 in the AD brain are not fully understood. Here, we review evidences related to the role of GLP-1 in type 3 diabetes.

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Brain

Cited by 102 publications

References 64 publications

Perimenopause and emergence of an Alzheimer’s bioenergetic phenotype in brain and periphery

Perimenopause and emergence of an Alzheimer’s bioenergetic phenotype in brain and periphery

Targeting Metabolism for Cancer Therapy

The Role of Glucagon-Like Peptide 1 (GLP1) in Type 3 Diabetes: GLP-1 Controls Insulin Resistance, Neuroinflammation and Neurogenesis in the Brain

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