Secretion of growth hormone and thyroid-stimulating hormone in patients with dementia

Gómez, José Manuel; Aguilar, Miquel; Navarro, M. A.; Ortolá, J; Soler, Joan

doi:10.1007/bf00207475

Cited by 13 publications

(4 citation statements)

References 23 publications

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“…Other alterations in the neuroendocrine system of AD patients have also been reported. An attenuated growth hormone-releasing hormone (GHRH) -induced growth hormone response specific to AD was demonstrated by Lesh et al (146) and Ghiso et al (147), but not by others (148,149). Furthermore, a reduction in CSF levels of antidiuretic hormone was observed not only in AD patients, but also in patients with frontal lobe dementia (150).…”

Section: Neuroendocrine Systemmentioning

confidence: 95%

Peripheral markers in testing pathophysiological hypotheses and diagnosing Alzheimer's disease

Gasparini¹,

Racchi²,

Binetti³

et al. 1998

FASEB j.

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Alterations in amyloid precursor protein (APP) metabolism, calcium regulation, oxidative metabolism, and transduction systems have been implicated in Alzheimer's disease (AD). Limitations to the use of postmortem brain for examining molecular mechanisms underscore the need to develop a human tissue model representative of the pathophysiological processes that characterize AD. The use of peripheral tissues, particularly of cultured skin fibroblasts derived from AD patients, could complement studies of autopsy samples and provide a useful tool with which to investigate such dynamic processes as signal transduction systems, ionic homeostasis, oxidative metabolism, and APP processing. Peripheral cells as well as body fluids (i.e., plasma and CSF) could also provide peripheral biological markers for the diagnosis of AD. The criteria required for a definite diagnosis of AD presently include clinical criteria in association with histopathologic evidence obtained from biopsy or autopsy. Thus, the use of peripheral markers as a diagnostic tool, either to predict or at least to confirm a diagnosis, may be of great importance. Gasparini, L., Racchi, M., Binetti, G., Trabucchi, M., Solerte, S. B., Alkon, D., Etcheberrigaray, R., Gibson, G., Blass, J., Paoletti, R., Govoni, S. Peripheral markers in testing pathophysiological hypotheses and diagnosing Alzheimer's disease. FASEB J. 12, 17–34 (1998)

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Section: Neuroendocrine Systemmentioning

confidence: 95%

Peripheral markers in testing pathophysiological hypotheses and diagnosing Alzheimer's disease

Gasparini¹,

Racchi²,

Binetti³

et al. 1998

FASEB j.

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“…Provocation test studies for GH have revealed controversial results. Gomez et al [19] reported no significant difference in GH levels between AD patients and controls when GH secretion is stimulated by GHRH. However, a lower GH response to GHRH in AD patients compared to controls was reported by Ghigo et al [18].…”

Section: Discussionmentioning

confidence: 99%

Decreased Plasma Insulin-Like Growth Factor-I Level in Familial Alzheimer’s Disease Patients Carrying the Swedish APP 670/671 Mutation

Mustafa

Lannfelt

Lilius

et al. 1999

Dement Geriatr Cogn Disord

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The plasma insulin-like growth factor I (IGF-I) level was determined in family members carrying the Swedish amyloid precursor protein (APP) 670/671 mutation with or without Alzheimer’s disease (AD) and in age-matched controls from the same family. Plasma growth hormone (GH) and prolactin (PRL) levels were also determined. Measurement of the plasma IGF-I level by radioimmunoassay revealed a significant reduction only in the family members with AD compared to age-matched controls. However, there was no significant difference in the levels of GH and PRL between the mutation carriers with or without AD and their respective age-matched controls. These findings indicate that the mechanism(s) regulating GH and PRL were preserved and those regulating IGF-I levels might be affected in AD patients with the Swedish APP 670/671 mutation.

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“…The results of several studies addressing this point show varied results [61,[65][66][67][68][69]: superimposable responses of GH to GHRH than responses in controls; a blunted GH to GHRH response in AD patients; higher GH concentrations in the morning; a greater increase of GH to GHRH in AD patients than in controls. In general, the investigations of GHreleasing stimulation tests, especially of GHRH in AD, are equivocal and in some cases contradictory [70][71][72].…”

Section: Growth Hormone Response To Stimuli In Alzheimer's Diseasementioning

confidence: 99%

Possible Usefulness of Growth Hormone/Insulin-like Growth Factor-I Axis in Alzheimer’s Disease Treatment

Sanchis

2012

EMIDDT

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Alzheimer's disease (AD) has been traditionally conceptualized as a clinicopathological entity, its definite diagnosis requiring the presence of characteristic pathology together with a dementia clinical picture. The fact that certain AD biomarkers show an acceptable sensitivity and specificity to detect AD pathology has shifted the diagnostic paradigm towards a clinicobiological approach. Neuropathological analysis of AD-affected brains reveals extensive atrophy due to neuronal loss, and accumulation of neurofibrillary tangles and neuritic plaques, surrounded by a tract of neuroinflammation and loss of neurons. Recently, emerging evidence supports the concept that AD is also a disorder of metabolic degeneration. Taken together, the neurochemical changes in the brain from patients with AD indicate multiple disturbances and it seems likely that the changes are secondary to more fundamental changes into the brain. There is a physiological decline of the growth hormone (GH)/insulin-like growth factor-I (IGF-I) axis with ageing and the possibility that the GH/ IGF-I axis is involved in cognitive deficits has been recognized for several years. The IGF-I is a potent neurotrophic as well neuroprotective factor found in the brain with a wide range of actions in both central and peripheral nervous system. IGF-I is a critical promoter of brain development and neuronal survival and plays a role in neuronal rescue during degenerative diseases. The investigations of GH releasing stimulation tests especially to GHRH in AD are equivocal and in some cases contradictory. When a cholinesterase inhibitor as rivastigmine, a drug for AD, is acutely administered the area under the curve of the GH response to GHRH doubled, showing that rivastigmine is a powerful drug to enhance GH release. Starting with a more accurate diagnosis not of the clinical syndrome, but of underlying molecular defects, that may eventually lead to a personalized, more effective treatment. Hence, the development of novel therapeutic approaches is urgently needed.

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Secretion of growth hormone and thyroid-stimulating hormone in patients with dementia

Cited by 13 publications

References 23 publications

Peripheral markers in testing pathophysiological hypotheses and diagnosing Alzheimer's disease

Peripheral markers in testing pathophysiological hypotheses and diagnosing Alzheimer's disease

Decreased Plasma Insulin-Like Growth Factor-I Level in Familial Alzheimer’s Disease Patients Carrying the Swedish APP 670/671 Mutation

Possible Usefulness of Growth Hormone/Insulin-like Growth Factor-I Axis in Alzheimer’s Disease Treatment

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