Causes and Consequences of Neuronal Energy Deficit in Sporadic Alzheimer's Disease

Bauer, Jens; Plaschke, Konstanze; Martin, Eike; Bardenheuer, H. J.; Hoyer, Siegfried

doi:10.1111/j.1749-6632.1997.tb48487.x

Cited by 8 publications

(6 citation statements)

References 7 publications

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“…In addition, it has been reported that TNF-· is able to promote neuron survival [41]. On the other hand, leptin and TNF-· could play a degenerative role by interfering with the insulin or insulin-like growth factor I (IGF-I) signal [42,43], thus contributing with the impaired glucose metabolism described in AD [9] and modulating the immune response, as proposed in other types of dementia [44]. AD certainly is a pathology associated with weight loss [45], however, the exact mechanisms linking AD and weight loss are still unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Leptin and TNF-· share, at least, two common properties: (1) they increase during the inflammatory process [6], and (2) they bind to the class 1 cytokine receptor family [7] inducing, among others, anorectic effects [8]. Interestingly, it has been reported [9] that weight loss precedes dementia in community-dwelling older adults. However, the elucidation of the role played by these two adipokines in the development of physiopathological events associated with AD still remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Although no prevalence by gender has been estimated for AD up to now, a higher risk for AD development in females than in males is evident for, among others, the longer life span of this sex. Because it is accepted that AD is a well-characterized eating disorder, the aim of the present study was to determine whether AD patients display any gender-related characteristic in several circulating eating-controlling metabolites that further could contribute to the eating disorder observed in AD patients [9].…”

Section: Introductionmentioning

confidence: 99%

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Alzheimer’s Disease Patients Display Gender Dimorphism in Circulating Anorectic Adipokines

Intebi¹,

Garau²,

Brusco³

et al. 2002

Neuroimmunomodulation

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Among neurodegenerative diseases, Alzheimer’s disease (AD) is a leading cause of death in elderly individuals. AD is characterized, among other clinical findings, by unexplained weight loss, cachexia and altered immune function. To explore whether any relationship between gender and circulating levels of several eating-controlling metabolites exist, we evaluated leptin, tumor necrosis factor (TNF)-α, triiodothyronine (T₃), free (F) thyroxine (T₄), TSH, PRL, insulin (INS), and cortisol in 15 AD-treated patients (age range 55–82 years): 9 postmenopausal females (without hormone replacement therapy) and 6 males. The results (mean ± SEM) indicated that circulating leptin levels were significantly (p < 0.05) higher in female AD (40.34 ± 11.1 ng/ml) than in male AD (6.07 ± 1.39 ng/ml) patients. The difference found in circulating leptin levels was noticed regardless of BMI (26.75 ± 1.77 and 24.55 ± 1.93 kg/m², in females and males, respectively) and waist:hip ratios (0.91 ± 0.03 and 0.94 ± 0.02, in females and males, respectively). Moreover, serum TNF-α concentrations were also significantly (p < 0.02) higher in AD females (12.24 ± 1.47 pg/ml) than in AD males (6.62 ± 1.44 pg/ml), regardless of TNF-α:BMI ratios (0.50 ± 0.09 and 0.28 ± 0.08, in females and males, respectively; p > 0.05). Finally, no differences were observed between gender (in female and male AD patients, respectively) in circulating levels of T₃ (151.33 ± 9.91 vs. 116 ± 17.04 ng/dl), FT₄ (1.26 ± 0.08 vs. 1.24 ± 0.06 ng/dl), TSH (1.28 ± 0.16 vs. 2.46 ± 0.67 µIU/ml), PRL (10.53 ± 2.47 vs. 12.61 ± 2.37 ng/ml), INS (11.76 ± 1.95 vs. 8.59 ± 1.34 µIU/ml) and cortisol (15.71 ± 1.23 vs. 12.63 ± 1.47 µg/dl). These results indicate that our AD group of patients, with normal corticoadrenal and thyroid functions and normoprolactinemia, displayed a gender-related characteristic in the circulating levels of two very important anorectic signals, leptin and TNF-α, being both higher in female than in male AD patients, regardless of BMI. Our study suggests that increased circulating levels of both anorexigenic adipokines may contribute to the metabolic changes observed in AD females.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Alzheimer’s Disease Patients Display Gender Dimorphism in Circulating Anorectic Adipokines

Intebi¹,

Garau²,

Brusco³

et al. 2002

Neuroimmunomodulation

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“…These mechano-functional abnormalities can lower the heart's ability to deliver the energy fuel necessary to meet the metabolic demands of brain cells, thus contributing to their potential death. [3][4][5][6] It would seem that during advanced aging, the heart can continue to be a good friend to the brain or become its insidious foe.…”

Section: Introductionmentioning

confidence: 97%

Cerebral Perfusion Enhancing Interventions: A New Strategy for the Prevention of Alzheimer Dementia

Torre

2016

Brain Pathology

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Cardiovascular and cerebrovascular diseases are major risk factors in the development of cognitive impairment and Alzheimer's disease (AD). These cardio-cerebral disorders promote a variety of vascular risk factors which in the presence of advancing age are prone to markedly reduce cerebral perfusion and create a neuronal energy crisis. Long-term hypoperfusion of the brain evolves mainly from cardiac structural pathology and brain vascular insufficiency. Brain hypoperfusion in the elderly is strongly associated with the development of mild cognitive impairment (MCI) and both conditions are presumed to be precursors of Alzheimer dementia. A therapeutic target to prevent or treat MCI and consequently reduce the incidence of AD aims to elevate cerebral perfusion using novel pharmacological agents. As reviewed here, the experimental pharmaca include the use of Rho kinase inhibitors, neurometabolic energy boosters, sirtuins and vascular growth factors. In addition, a compelling new technique in laser medicine called photobiomodulation is reviewed. Photobiomodulation is based on the use of low level laser therapy to stimulate mitochondrial energy production non-invasively in nerve cells. The use of novel pharmaca and photobiomodulation may become important tools in the treatment or prevention of cognitive decline that can lead to dementia.

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“…Alzheimer’s disease (AD) is accompanied by a disturbance in energy metabolism that has been proposed as a primary pathophysiologic factor [1, 2, 3]. In previous work, we reported abnormal elevations in plasma insulin in patients with AD, both in fasting states and after glucose tolerance testing, suggesting defective insulin action.…”

Section: Introductionmentioning

confidence: 99%

Insulin Metabolism in Alzheimer’s Disease Differs According to Apolipoprotein E Genotype and Gender

et al. 1999

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Higher fasting plasma insulin levels and reduced CSF-to-plasma insulin ratios, suggestive of insulin resistance, have been observed in patients with Alzheimer’s disease (AD) who do not possess an apolipoprotein E (APOE)-Ε4 allele. We examined the relationship of APOE and gender to peripheral insulin action and hyperinsulinemic memory facilitation in patients with AD using a sensitive measure of insulin-mediated glucose disposal. Participants were 32 patients with AD (9 without an Ε4 allele, 23 with an Ε4 allele) and 25 healthy age-matched adults (16 without an Ε4 allele, 9 with an Ε4 allele). AD subjects without an Ε4 allele had significantly lower insulin-mediated glucose disposal rates than AD patients with an Ε4 allele (p < 0.03), or than normal adults without an Ε4 allele (p < 0.02). Female AD subjects showed lower insulin-mediated glucose disposal rates than did male AD subjects (p < 0.02). No significant interaction was observed between APOE group and gender, suggesting that these effects are independent. AD subjects without an Ε4 allele also showed significant memory facilitation in the hyperinsulinemic condition (p < 0.04), whereas the AD-Ε4 group did not. Also in the hyperinsulinemic condition, AD patients without an Ε4 allele had lower insulin levels than patients with an Ε4 allele (p < 0.02), and women with AD had lower insulin levels than did men with AD despite similar insulin infusion rates and body mass (p < 0.004). No gender or genotype effects were observed in either condition for normal subjects. These results provide in vivo evidence of differences in insulin-mediated energy metabolism between Ε4 and non-Ε4 AD, and suggest that defective insulin action may be of particular pathophysiologic significance for patients without an Ε-4 allele.

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Causes and Consequences of Neuronal Energy Deficit in Sporadic Alzheimer's Disease

Cited by 8 publications

References 7 publications

Alzheimer’s Disease Patients Display Gender Dimorphism in Circulating Anorectic Adipokines

Alzheimer’s Disease Patients Display Gender Dimorphism in Circulating Anorectic Adipokines

Cerebral Perfusion Enhancing Interventions: A New Strategy for the Prevention of Alzheimer Dementia

Insulin Metabolism in Alzheimer’s Disease Differs According to Apolipoprotein E Genotype and Gender

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