Somatomedins in aging and dementia disorders of the Alzheimer type

Sara, Vicki R.; Hall, Kerstin; Enzell, Karin; Gardner, Ann; Morawski, Richard; Wetterberg, Lennart

doi:10.1016/0197-4580(82)90006-9

Cited by 39 publications

(13 citation statements)

References 11 publications

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“…Additionally the IGFBP levels in CSF were found to be highly significantly elevated. These results are in accordance with previous studies suggesting both an alteration of CSF and serum IGF activity in AD (Sara et al, 1982). In both the patient group and in the subjects CSF immunoreactive "big" IGF-2, IGF-2 and IGF-1 was identified and the levels were similar to previous reports (Haselbacher and Humbel, 1982).…”

Section: Discussionsupporting

confidence: 95%

“…Earlier studies have shown that unseparated whole CSF from AD display increased IGF radio-receptoractivity. These findings were most likely due to elevated IGFBPs (Sara et al, 1982). Accordingly, Tham et al (1988) observed elevated activity corresponding to IGFBP, "big" IGF-2 and IGF-2 in a single pooled sample of AD CSF following acidification and chromatografic separation.…”

Section: Introductionmentioning

confidence: 81%

“…The IGFs have been suggested to play a role in neurodegenerative disorders (Sara et al, 1982). Earlier studies have shown that unseparated whole CSF from AD display increased IGF radio-receptoractivity.…”

Section: Introductionmentioning

confidence: 99%

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Insulin-like growth factors and insulin-like growth factor binding proteins in cerebrospinal fluid and serum of patients with dementia of the Alzheimer type

Tham

Nordberg

Grissom

et al. 1993

J Neural Transm Gen Sect

135

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After acid gel-chromatography cerebrospinal fluid and serum levels of immunoreactive insulin-like growth factor 1 and 2 (IGF-1 and IGF-2) were determined in patients with dementia of the Alzheimer type (AD) and in healthy subjects. The AD CSF levels of immunoreactive IGF-1 did not differ from the subjects but the levels of immunoreactive IGF-2 was significantly elevated in both serum and CSF in the AD patient group. Additionally immunoreactive IGF-1 in AD serum was found to be significantly elevated. To characterize the CSF IGF binding protein activity (IGFBP), ligand blotting was performed on whole CSF from AD patients and subjects. The results demonstrate two major forms of IGFBP in CSF with approximate molecular weights of 33 KDa and 30 KDa. The two IGFBP forms are suggested to represent IGFBP-2 and IGFBP-6. A highly significant increase in both the IGFBPs was observed in the CSF of the AD patients compared to the healthy subjects.

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Section: Discussionsupporting

confidence: 95%

Section: Introductionmentioning

confidence: 81%

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Insulin-like growth factors and insulin-like growth factor binding proteins in cerebrospinal fluid and serum of patients with dementia of the Alzheimer type

Tham

Nordberg

Grissom

et al. 1993

J Neural Transm Gen Sect

135

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“…An increase in the GHRH-induced GH release after pretreatment with PD in demented patients has been reported recently [17], It is widely accepted that GH secretion declines with age in humans [20][21][22] so that normal elderly subjects have GH and IGF-I levels similar to those of patients with GH deficiency [20,21], In patients with AD basal GH levels similar [15,23, 24] or higher [23] than those in agematched normal elderly subjects have been reported. Moreover, in AD, IGF-I concentrations have been found to be low, but higher than those recorded in age-matched controls [25,26]. In the present study we found basal GH levels overlapping in the three groups, while IGF-I con centrations in AD were lower than in young adults but higher than in normal age-matched controls.…”

Section: Discussionsupporting

confidence: 50%

Growth Hormone Secretion in Alzheimer's Disease: Studies with Growth Hormone-Releasing Hormone Alone and Combined with Pyridostigmine or Arginine

Ghigo

Nicolosi

Arvat

et al. 1993

Dement Geriatr Cogn Disord

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There is evidence that GH secretion is reduced in normal elderly subjects as well as in patients with Alzheimer''s disease (AD). To clarify the mechanisms underlying this GH hyposecretory state in 14 elderly subjects (age 65–75 years) and 15 AD patients (age 61–78 years), we studied the effects of both pyridostigmine (PD, 120 mg orally), a cholinesterase inhibitor, and arginine (ARG, 0.5 g/kg i.v.), two substances likely acting via inhibition of hypothalamic somatostatin, on GH response to GHRH (1 (µg/kg i.v.). The GH response to PD alone was also studied. Twenty-two young healthy volunteers were studied as control group. Basal GH levels were similar in young, elderly and AD subjects (0.7 ± 0.2, 0.8 ± 0.2 and 0.9 ± 0.2 µg/1). IGF-I levels were lower (p < 0.005) in elderly (73.9 ± 8.2 µg/1) and in AD subjects (108.0 ± 5.9 µg/l) than in young subjects (288.7 ± 22.1 µg/l); however, they were higher (p < 0.01) in AD patients than in the elderly subjects. The PD-induced GH release did not significantly differ in young, elderly and AD subjects while the GH responses to GHRH in the elderly (AUC: 297.9 ± 49.2 µg/l/h) and in AD subjects (437.6 ± 93.5 µg/l/h) were lower (p < 0.01) than in young subjects (658.6 ± 100.1 µg/l/h). PD potentiated the GH response to GHRH both in elderly and in AD subjects (901.7 ± 222.4 and 1,070.3 ± 207.2 µg/l/h, p < 0.005) but these responses were lower (p < 0.0001) than those recorded in young subjects (2,041.1 ± 245.6 µg/l/h). ARG potentiated the GHRH-induced GH rise both in elderly and in AD subjects (1,545.2 ± 246.0 and 1,659.3 ± 196.8 µg/l/h,p < 0.001) but in this case, the GH response to GHRH + ARG overlapped with that in young subjects (2,140.2 ± 229.5 µg/l/h). In contrast to young subjects, in elderly and in AD subjects, the potentiating effect of ARG on GHRH-induced GH rise was higher (p < 0.01) than that of PD. These results show that testing neural controls of GH secretion with different neuroactive substances does not allow to differentiate normal aging from AD. In both groups, somatotroph responsiveness to GHRH is potentiated by the enhancement of the cholinergic activity but much more by ARG, which is compatible with the presence of a cholinergic impairments.

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“…IGFs have been assumed to play a role in AD [9,10]. It has been reported that the IGF-I level is elevated in the serum but not in cerebrospinal fluid of AD patients [11].…”

Section: Introductionmentioning

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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Somatomedins in aging and dementia disorders of the Alzheimer type

Cited by 39 publications

References 11 publications

Insulin-like growth factors and insulin-like growth factor binding proteins in cerebrospinal fluid and serum of patients with dementia of the Alzheimer type

Insulin-like growth factors and insulin-like growth factor binding proteins in cerebrospinal fluid and serum of patients with dementia of the Alzheimer type

Growth Hormone Secretion in Alzheimer's Disease: Studies with Growth Hormone-Releasing Hormone Alone and Combined with Pyridostigmine or Arginine

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

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