Kooperativer Bibliotheksverbund

Berlin Brandenburg

and
and

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Copani, Agata  (63)
Type of Medium
Language
Year
  • 1
    Language: English
    In: European Journal of Pharmacology, Jan 10, 2010, Vol.626(1), p.64(8)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ejphar.2009.10.022 Byline: Filippo Caraci (a), Agata Copani (a)(b), Ferdinando Nicoletti (c)(d), Filippo Drago (e) Keywords: Major depression; Alzheimer's disease; Chronic inflammation; [beta]-amyloid; Transforming-growth-factor-[beta]1; Brain-derived neurotrophic factor; Neuroprotection Abstract: Depression is one of the most prevalent and life-threatening forms of mental illnesses, whereas Alzheimer's disease is a neurodegenerative disorder that affects more than 37 million people worldwide. Recent evidence suggests a strong relationship between depression and Alzheimer's disease. A lifetime history of major depression has been considered as a risk factor for later development of Alzheimer's disease. The presence of depressive symptoms can affect the conversion of mild cognitive impairment into Alzheimer's disease. Neuritic plaques and neurofibrillary tangles, the two major hallmarks of Alzheimer's disease brain, are more pronounced in the brains of Alzheimer's disease patients with comorbid depression as compared with Alzheimer's disease patients without depression. On the other hand, neurodegenerative phenomena have been observed in different brain regions of patients with a history of depression. Recent evidence suggests that molecular mechanisms and cascades that underlie the pathogenesis of major depression, such as chronic inflammation and hyperactivation of hypothalamic-pituitary-adrenal (HPA) axis, are also involved in the pathogenesis of Alzheimer's disease. In particular, a specific impairment in the signaling of some neurotrophins such as transforming-growth-factor [beta]1 (TGF-[beta]1) and brain-derived neurotrophic factor (BDNF) has been observed both in depression and Alzheimer's disease. In the present review we will examine the evidence on the common molecular pathways between depression and Alzheimer's disease and we will discuss these pathways as new pharmacological targets for the treatment of both major depression and Alzheimer's disease. Author Affiliation: (a) Department of Pharmaceutical Sciences, University of Catania, 95125, Catania, Italy (b) I.B.B., CNR-Catania, 95125, Catania, Italy (c) I.N.M. Neuromed, Localita Camerelle, 86077, Pozzilli, Italy (d) Department of Human Physiology and Pharmacology, University of Rome La Sapienza, 00185 Rome, Italy (e) Department of Experimental and Clinical Pharmacology, University of Catania, 95125, Catania, Italy Article History: Accepted 9 October 2009
    Keywords: Depression (Mood disorder) -- Risk Factors ; Depression (Mood disorder) -- Development And Progression ; Alzheimer's Disease -- Risk Factors ; Alzheimer's Disease -- Development And Progression ; Peptide Hormones ; Transforming Growth Factors ; Brain
    ISSN: 0014-2999
    Source: Cengage Learning, Inc.
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Language: English
    In: European Journal of Pharmacology, 10 January 2010, Vol.626(1), pp.64-71
    Description: Depression is one of the most prevalent and life-threatening forms of mental illnesses, whereas Alzheimer's disease is a neurodegenerative disorder that affects more than 37 million people worldwide. Recent evidence suggests a strong relationship between depression and Alzheimer's disease. A lifetime history of major depression has been considered as a risk factor for later development of Alzheimer's disease. The presence of depressive symptoms can affect the conversion of mild cognitive impairment into Alzheimer's disease. Neuritic plaques and neurofibrillary tangles, the two major hallmarks of Alzheimer's disease brain, are more pronounced in the brains of Alzheimer's disease patients with comorbid depression as compared with Alzheimer's disease patients without depression. On the other hand, neurodegenerative phenomena have been observed in different brain regions of patients with a history of depression. Recent evidence suggests that molecular mechanisms and cascades that underlie the pathogenesis of major depression, such as chronic inflammation and hyperactivation of hypothalamic–pituitary–adrenal (HPA) axis, are also involved in the pathogenesis of Alzheimer's disease. In particular, a specific impairment in the signaling of some neurotrophins such as transforming-growth-factor β1 (TGF-β1) and brain-derived neurotrophic factor (BDNF) has been observed both in depression and Alzheimer's disease. In the present review we will examine the evidence on the common molecular pathways between depression and Alzheimer's disease and we will discuss these pathways as new pharmacological targets for the treatment of both major depression and Alzheimer's disease.
    Keywords: Major Depression ; Alzheimer'S Disease ; Chronic Inflammation ; Β-Amyloid ; Transforming-Growth-Factor-Β1 ; Brain-Derived Neurotrophic Factor ; Neuroprotection ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0014-2999
    E-ISSN: 1879-0712
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Language: English
    In: Molecular Pain, Jan 14, 2011, Vol.7, p.6
    Description: Group II metabotropic glutamate receptors (mGluRs) couple to the inhibitory G-protein Gi. The group II mGluRs include two subtypes, mGlu2 and mGlu3, and their pharmacological activation produces analgesic effects in inflammatory and neuropathic pain states. However, the specific contribution of each one of the two subtypes has not been clarified due to the lack of selective orthosteric ligands that can discriminate between mGlu2 and mGlu3 subtypes. In this study we used mGlu2 or mGlu3 knock-out mice to dissect the specific role for these two receptors in the endogenous control of inflammatory pain and their specific contribution to the analgesic activity of mixed mGlu2/3 receptor agonists. Our results showed that mGlu2.sup.-/- .sup.mice display a significantly greater pain response compared to their wild type littermates. Interestingly the increased pain sensitivity in mGlu2.sup.-/- .sup.mice occurred only in the second phase of the formalin test. No differences were observed in the first phase. In contrast, mGlu3.sup.-/- .sup.mice did not significantly differ from their wild type littermates in either phase of the formalin test. When systemically injected, a single administration of the mGlu2/3 agonist, LY379268 (3 mg/kg, ip), showed a significant reduction of both phases in wild-type mice and in mGlu3.sup.-/- .sup.but not in mGlu2.sup.-/- .sup.mice. However tolerance to the analgesic effect of LY379268 (3 mg/kg, ip) in mGlu3.sup.-/- .sup.mice developed following 5 consecutive days of injection. Taken together, these results demonstrate that: (i) mGlu2 receptors play a predominant role over mGlu3 receptors in the control of inflammatory pain in mice; (ii) the analgesic activity of mixed mGlu2/3 agonists is entirely mediated by the activation of the mGlu2 subtype and (iii) the development of tolerance to the analgesic effect of mGlu2/3 agonists develops despite the lack of mGlu3 receptors.
    Keywords: Glutamate -- Physiological Aspects ; Glutamate -- Genetic Aspects ; Glutamate -- Research ; Pain Management -- Physiological Aspects ; Pain Management -- Genetic Aspects ; Pain Management -- Research ; Cell Receptors -- Physiological Aspects ; Cell Receptors -- Genetic Aspects ; Cell Receptors -- Research
    ISSN: 1744-8069
    Source: Cengage Learning, Inc.
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Language: English
    In: Molecular Pain, Jan 14, 2011, Vol.7, p.6
    Description: Group II metabotropic glutamate receptors (mGluRs) couple to the inhibitory G-protein Gi. The group II mGluRs include two subtypes, mGlu2 and mGlu3, and their pharmacological activation produces analgesic effects in inflammatory and neuropathic pain states. However, the specific contribution of each one of the two subtypes has not been clarified due to the lack of selective orthosteric ligands that can discriminate between mGlu2 and mGlu3 subtypes. In this study we used mGlu2 or mGlu3 knock-out mice to dissect the specific role for these two receptors in the endogenous control of inflammatory pain and their specific contribution to the analgesic activity of mixed mGlu2/3 receptor agonists. Our results showed that mGlu2.sup.-/- .sup.mice display a significantly greater pain response compared to their wild type littermates. Interestingly the increased pain sensitivity in mGlu2.sup.-/- .sup.mice occurred only in the second phase of the formalin test. No differences were observed in the first phase. In contrast, mGlu3.sup.-/- .sup.mice did not significantly differ from their wild type littermates in either phase of the formalin test. When systemically injected, a single administration of the mGlu2/3 agonist, LY379268 (3 mg/kg, ip), showed a significant reduction of both phases in wild-type mice and in mGlu3.sup.-/- .sup.but not in mGlu2.sup.-/- .sup.mice. However tolerance to the analgesic effect of LY379268 (3 mg/kg, ip) in mGlu3.sup.-/- .sup.mice developed following 5 consecutive days of injection. Taken together, these results demonstrate that: (i) mGlu2 receptors play a predominant role over mGlu3 receptors in the control of inflammatory pain in mice; (ii) the analgesic activity of mixed mGlu2/3 agonists is entirely mediated by the activation of the mGlu2 subtype and (iii) the development of tolerance to the analgesic effect of mGlu2/3 agonists develops despite the lack of mGlu3 receptors.
    Keywords: Glutamate -- Physiological Aspects ; Glutamate -- Genetic Aspects ; Glutamate -- Research ; Pain Management -- Physiological Aspects ; Pain Management -- Genetic Aspects ; Pain Management -- Research ; Cell Receptors -- Physiological Aspects ; Cell Receptors -- Genetic Aspects ; Cell Receptors -- Research
    ISSN: 1744-8069
    Source: Cengage Learning, Inc.
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Language: English
    In: Molecular Pain, 14 January 2011, Vol.7
    Description: Group II metabotropic glutamate receptors (mGluRs) couple to the inhibitory G-protein Gi. The group II mGluRs include two subtypes, mGlu2 and mGlu3, and their pharmacological activation produces analgesic effects in inflammatory and neuropathic pain states. However, the specific contribution of each one of the two subtypes has not been clarified due to the lack of selective orthosteric ligands that can discriminate between mGlu2 and mGlu3 subtypes. In this study we used mGlu2 or mGlu3 knock-out mice to dissect the specific role for these two receptors in the endogenous control of inflammatory pain and their specific contribution to the analgesic activity of mixed mGlu2/3 receptor agonists. Our results showed that mGlu2−/− mice display a significantly greater pain response compared to their wild type littermates. Interestingly the increased pain sensitivity in mGlu2−/− mice occurred only in the second phase of the formalin test. No differences were observed in the first phase. In contrast, mGlu3−/− mice did not significantly differ from their wild type littermates in either phase of the formalin test. When systemically injected, a single administration of the mGlu2/3 agonist, LY379268 (3 mg/kg, ip), showed a significant reduction of both phases in wild-type mice and in mGlu3−/− but not in mGlu2−/− mice. However tolerance to the analgesic effect of LY379268 (3 mg/kg, ip) in mGlu3−/− mice developed following 5 consecutive days of injection. Taken together, these results demonstrate that: (i) mGlu2 receptors play a predominant role over mGlu3 receptors in the control of inflammatory pain in mice; (ii) the analgesic activity of mixed mGlu2/3 agonists is entirely mediated by the activation of the mGlu2 subtype and (iii) the development of tolerance to the analgesic effect of mGlu2/3 agonists develops despite the lack of mGlu3 receptors.
    Keywords: Medicine ; Anatomy & Physiology
    ISSN: 1744-8069
    E-ISSN: 1744-8069
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Language: English
    In: PLoS ONE, 01 January 2011, Vol.6(1), p.e16447
    Description: The identification of mechanisms that mediate stress-induced hippocampal damage may shed new light into the pathophysiology of depressive disorders and provide new targets for therapeutic intervention. We focused on the secreted glycoprotein...
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Language: English
    In: Current Opinion in Pharmacology, February 2018, Vol.38, pp.1-7
    Description: A dysfunction of glutamate signaling is implicated at several levels in the pathogenesis of Alzheimer's disease. Currently, metabotropic glutamate receptors, which have a wide distribution in the central nervous system and activate a multitude of cell signaling pathways, are pursued as targets for therapeutic intervention in Alzheimer's disease. Research is still limited, but results underscore the relevance of ongoing studies. Here we discuss the latest updates regarding metabotropic glutamate receptors and their role in Alzheimer's disease, as well as promising metabotropic glutamate receptor ligands that have been investigated in preclinical models of Alzheimer's disease.
    Keywords: Pharmacy, Therapeutics, & Pharmacology
    ISSN: 1471-4892
    E-ISSN: 1471-4973
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Language: English
    In: Cell and Tissue Research, Jan, 2012, Vol.347(1), p.291(11)
    Description: Abstract Alzheimer's disease (AD) is a neurodegenerative disorder that affects about 35 million people worldwide. Current drugs for AD only treat the symptoms and do not interfere with the underlying pathogenic mechanisms of the disease. AD is characterized by the presence of [beta]-amyloid (A[beta]) plaques, neurofibrillary tangles, and neuronal loss. Identification of the molecular determinants underlying Ferdinando Nicoletti and Agata Copani are co-senior authors. A[beta]-induced neurodegeneration is an essential step for the development of disease-modifying drugs. Recently, an impairment of the transforming growth factor-[beta]1 (TGF[beta]1) signaling pathway has been demonstrated to be specific to the AD brain and, particularly, to the early phase of the disease. TGF-[beta]1 is a neurotrophic factor responsible for the initiation and maintenance of neuronal differentiation and synaptic plasticity. The deficiency of TGF-[beta]1 signaling is associated with A[beta] pathology and neurofibrillary tangle formation in AD animal models. Reduced TGF-[beta]1 signaling seems to contribute both to microglial activation and to ectopic cell-cycle re-activation in neurons, two events that contribute to neurodegeneration in the AD brain. The neuroprotective features of TGF-[beta]1 indicate the advantage of rescuing TGF-[beta]1 signaling as a means to slow down the neurodegenerative process in AD. Keywords Alzheimer's disease * [beta]-Amyloid * Transforming growth factor-[beta]1 * Apoptosis * Cell cycle activation. Neuroprotection
    Keywords: Alzheimer's Disease -- Development And Progression ; Bone Morphogenetic Proteins ; Amyloid Beta-protein ; Transforming Growth Factors
    ISSN: 0302-766X
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    Language: English
    In: Frontiers in Molecular Neuroscience, Nov 13, 2018
    Description: Neurodegenerative disorders are characterized by excitotoxicity and neuroinflammation that finally lead to slow neuronal degeneration and death. Although neurons are the principal target, glial cells are important players as they contribute by either exacerbating or dampening the events that lead to neuroinflammation and neuronal damage. A dysfunction of the glutamatergic system is a common event in the pathophysiology of these diseases. Metabotropic glutamate (mGlu) receptors belong to a large family of G protein-coupled receptors largely expressed in neurons as well as in glial cells. They often appear overexpressed in areas involved in neurodegeneration, where they can modulate glutamatergic transmission. Of note, mGlu receptor upregulation may involve microglia or, even more frequently, astrocytes, where their activation causes release of factors potentially able to influence neuronal death. The expression of mGlu receptors has been also reported on oligodendrocytes, a glial cell type specifically involved in the development of multiple sclerosis. Here we will provide a general overview on the possible involvement of mGlu receptors expressed on glial cells in the pathogenesis of different neurodegenerative disorders and the potential use of subtype-selective mGlu receptor ligands as candidate drugs for the treatment of neurodegenerative disorders. Negative allosteric modulators (NAM) of mGlu5 receptors might represent a relevant pharmacological tool to develop new neuroprotective strategies in these diseases. Recent evidence suggests that targeting astrocytes and microglia with positive allosteric modulators (PAM) of mGlu3 receptor or oligodendrocytes with mGlu4 PAMS might represent novel pharmacological approaches for the treatment of neurodegenerative disorders.
    Keywords: Glutamate ; Nervous System Diseases
    ISSN: 1662-5099
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    Language: English
    In: Neuropharmacology, 15 March 2017, Vol.115, pp.180-192
    Description: Metabotropic glutamate (mGlu) receptor ligands are under clinical development for the treatment of CNS disorders with high social and economic burden, such as schizophrenia, major depressive disorder (MDD), and Parkinson’s disease (PD), and are promising drug candidates for the treatment of Alzheimer’s disease (AD). So far, clinical studies have shown symptomatic effects of mGlu receptor ligands, but it is unknown whether these drugs act as disease modifiers or, at the opposite end, they accelerate disease progression by enhancing neurodegeneration. This is a fundamental issue in the treatment of PD and AD, and is also an emerging theme in the treatment of schizophrenia and MDD, in which neurodegeneration is also present and contribute to disease progression. Moving from data and preclinical studies, we discuss the potential impact of drugs targeting mGlu2, mGlu3, mGlu4 and mGlu5 receptor ligands on active neurodegeneration associated with AD, PD, schizophrenia, and MDD. We wish to highlight that our final comments on the best drug candidates are not influenced by commercial interests or by previous or ongoing collaborations with drug companies. This article is part of the Special Issue entitled ‘Metabotropic Glutamate Receptors, 5 years on’.
    Keywords: Metabotropic Glutamate Receptors ; Schizophrenia ; Major Depressive Disorders ; Alzhiemer’s Disease ; Parkinson’s Disease ; Neurodegeneration ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages