Quantitative autoradiography of [3H]forskolin binding sites in post-mortem brain staged for Alzheimer's disease neurofibrillary changes and amyloid deposits

García-Jiménez, Angela; Cowburn, Richard F.; Ohm, Thomas G.; Bogdanović, Nenad; Winblad, Bengt; Fastbom, Johan

doi:10.1016/s0006-8993(99)02111-3

Cited by 19 publications

(4 citation statements)

References 43 publications

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“…Continuous intracerebroventricular infusion of Ab25-35 did not alter either basal or forskolin-stimulated AC activity in rat cortical membranes. This finding is in accordance with some data in AD post-mortem brains (Bonkale et al 1996), while others report a decrease in AC activity (García-Jiménez et al 1999). This discrepancy could be because of an anatomically specific effect of Ab as some cerebral areas show alterations in AC activity, whereas others do not .…”

Section: Discussionsupporting

confidence: 91%

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Protective effects of insulin‐like growth factor‐I on the somatostatinergic system in the temporal cortex of β‐amyloid‐treated rats

Aguado-Llera

Arilla‐Ferreiro

Campos‐Barros

et al. 2004

Journal of Neurochemistry

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Insulin-like growth factor-I (IGF-I) has protective effects against b-amyloid (Ab)-induced neuronal cell death. Because alterations of the somatostatinergic system have been described in Alzheimer's disease, we investigated the effects of the Ab peptide and the possible protective role of IGF-I on the somatostatinergic system of the rat temporal cortex and on cell death and phosphorylated (p)-Akt levels in this area. Ab25-35 was administered intracerebroventricularly to male rats via an osmotic minipump over 14 days (300 pmol/day). Another group received a subcutaneous IGF-I infusion (50 lg/kg/day), concomitant with Ab25-35 administration, whereas a third group received IGF-I alone. Ab25-35 significantly decreased the somatostatin (SRIF)-like immunoreactive content and the SRIF receptor density, as a result of a decrease in the levels of the SRIF receptor subtype 2. The inhibitory effect of SRIF on adenylyl cyclase activity was significantly lower after Ab25-35 infusion, whereas the levels of the inhibitory G protein subunit Gia1, Gia2 or Gia3 were unaltered. Cell death was increased and p-Akt levels decreased in Ab25-35-treated animals. IGF-I administration increased immunoreactive IGF-I levels in the temporal cortex and restored all parameters affected by Ab25-35 to baseline values. These findings suggest that IGF-I prevents the deleterious effect of Ab25-35 on the somatostatinergic system.

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Section: Discussionsupporting

confidence: 91%

“…This finding is in accordance with some data in AD post‐mortem brains (Bonkale et al . 1996), while others report a decrease in AC activity (García‐Jiménez et al . 1999).…”

Section: Discussionmentioning

confidence: 94%

Protective effects of insulin‐like growth factor‐I on the somatostatinergic system in the temporal cortex of β‐amyloid‐treated rats

Aguado-Llera

Arilla‐Ferreiro

Campos‐Barros

et al. 2004

Journal of Neurochemistry

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“…cAMP and especially its main target protein kinase, PKA, are thought to play a role in the etiology of neurofibrillary tangles via phosphorylation of tau (25, 26). A downregulation of the AC/cAMP/PKA signaling pathway has been reported in human patients with AD (27–29). As a main activator of CREB, a decrease in AC/cAMP/PKA signaling can also account for loss in synaptic plasticity and memory decline in AD (30).…”

Section: Neurodegenerative Disordersmentioning

confidence: 99%

Phosphodiesterases in neurodegenerative disorders

2012

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SummaryCyclic nucleotide phosphodiesterases (PDEs) are responsible for the breakdown of cyclic nucleotides, cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). As such, they are crucial regulators of levels of cyclic nucleotide-mediated signaling. cAMP signaling and cGMP signaling have been associated with neuroplasticity and protection, and influencing their levels in the cell by inhibition of PDEs has become a much studied target for treatment in a wide array of disorders, including neurodegenerative disorders. In this review, we will focus on the involvement of PDEs in neurodegenerative disorders. In comparison with preclinical work, data on human patients are scarce. Alzheimer's disease is associated with changes in PDE4, PDE7, and PDE8 expression in the brain. Altered functioning of PDE4 as well as PDE11 is associated with major depressive disorder. In multiple sclerosis, there are indications of alterations in expression of several PDE subtypes in the central nervous system; however, evidence is indirect. In Huntington's disease and Parkinson's disease, most research has focused on PDE1B and PDE10, because of their abundant presence in striatal neurons. In another rare, neurodegenerative striatal motor disorder, that is, autosomal-dominant striatal degeneration, genetic defects in PDE8B gene are thought to underlie the neurodegenerative processes. Although the latter disorder has showed a causative dysfunction of PDEs, this does not hold for the neurodegenerative disorders discussed above, in which changes in PDE levels seemingly rather represent secondary changes and compensation to prior existing dysfunction. However, normalizing cyclic nucleotide signaling via PDE inhibition remains interesting for the treatment of neurodegenerative disorders.2012 IUBMB IUBMB Life, 64(12): 965-970, 2012

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“…Studies of the functional activity of a receptorYG-proteinYsecond messenger system may be performed in vitro on postmortem tissue from subjects who suffered from neurodegenerative disorders using [ 3 H] forskolin binding or G-protein binding assays using [ 3 H]Gpp(NH)p or [ 35 S]GTPgS. It has been shown that [ 3 H]forskolin binding is decreased in tissue from the entorhinal cortex of subjects with AD, a decrease that is correlated to staging for neurofibrillary changes [46]. Moreover, the same group reported a significant decrease in the ability of GTP to stimulate the binding of [ 35 ]SGTPgS to the G-protein.…”

Section: Imaging Receptors Transporters and Other Components In Neumentioning

confidence: 99%

In Vitro Imaging Techniques in Neurodegenerative Diseases

Långström

Andrén

Lindhe³

et al. 2007

Mol Imaging Biol

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Neurodegeneration induces various changes in the brain, changes that may be investigated using neuroimaging techniques. The in vivo techniques are useful for the visualization of major changes, and the progressing abnormalities may also be followed longitudinally. However, to study and quantify minor abnormalities, neuroimaging of postmortem brain tissue is used. These in vitro methods are complementary to the in vivo techniques and contribute to the knowledge of pathophysiology and etiology of the neurodegenerative diseases. In vitro radioligand autoradiography has given great insight in the involvement of different neuronal receptor systems in these diseases. Data on the dopamine and cholinergic systems in neurodegeneration are discussed in this review. Also, the amyloid plaques are studied using in vitro radioligand autoradiography. Using one of the newer methods, imaging matrix-assisted laser desorption ionization mass spectrometry, the distribution of a large number of peptides and proteins may be detected in vitro on brain cryosections. In this overview, we describe in vitro imaging techniques in the neurodegenerative diseases as a complement to in vivo positron emission tomography and single photon emission computed tomography imaging.

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Quantitative autoradiography of [3H]forskolin binding sites in post-mortem brain staged for Alzheimer's disease neurofibrillary changes and amyloid deposits

Cited by 19 publications

References 43 publications

Protective effects of insulin‐like growth factor‐I on the somatostatinergic system in the temporal cortex of β‐amyloid‐treated rats

Protective effects of insulin‐like growth factor‐I on the somatostatinergic system in the temporal cortex of β‐amyloid‐treated rats

Phosphodiesterases in neurodegenerative disorders

In Vitro Imaging Techniques in Neurodegenerative Diseases

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