The neuroprotective effects of GLP-1: Possible treatments for cognitive deficits in individuals with mood disorders
Identifieur interne : 000110 ( PascalFrancis/Corpus ); précédent : 000109; suivant : 000111The neuroprotective effects of GLP-1: Possible treatments for cognitive deficits in individuals with mood disorders
Auteurs : Roger S. Mcintyre ; Alissa M. Powell ; Oksana Kaidanovich-Beilin ; Joanna K. Soczynska ; Mohammad Alsuwaidan ; Hanna O. Woldeyohannes ; Ashley S. Kim ; L. Ashley GallaugherSource :
- Behavioural brain research [ 0166-4328 ] ; 2013.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Incretins are a group of gastrointestinal hormones detected both peripherally and in the central nervous system (CNS). Recent studies have documented multiple effects of incretins on brain structure and function. Research into the neurological effects of incretins has primarily focused on animal models of neurodegenerative disorders (e.g., Alzheimer's Disease, Huntington's and Parkinson's diseases). Mood disorders (e.g. bipolar disorder (BD), major depressive disorder (MDD)) are associated with similar alterations in brain structure and function, as well as a range of cognitive deficits (e.g. memory, learning, executive function). Brain abnormalities and cognitive deficits are also found in populations with metabolic disorders (e.g., diabetes mellitus Type 2). In addition, individuals with mood disorders often have co-morbid metabolic conditions, thus treatment strategies which can effectively treat both cognitive deficits and metabolic abnormalities represent a possible integrated treatment avenue. In particular, glucagon-like peptide-1 (GLP-1 ) and its more stable, longer-lasting analogues have been demonstrated to exert neuroprotective and anti-apoptotic effects, reduce beta-amyloid (Aβ) plaque accumulation, modulate long-term potentiation and synaptic plasticity, and promote differentiation of neuronal progenitor cells. In animal models of behaviour, treatment with GLP-1 receptor agonists has been demonstrated to improve measures of cognitive function including learning and memory, as well as reduce depressive behaviour. Available GLP-1 treatments also have a favourable metabolic profile which includes weight loss and reduced risk for hypoglycemia. Systematic evaluation of the effects of GLP-1 treatment in psychiatric populations who evince cognitive deficits represents a promising treatment avenue.
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Format Inist (serveur)
NO : | PASCAL 13-0122012 INIST |
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ET : | The neuroprotective effects of GLP-1: Possible treatments for cognitive deficits in individuals with mood disorders |
AU : | MCINTYRE (Roger S.); POWELL (Alissa M.); KAIDANOVICH-BEILIN (Oksana); SOCZYNSKA (Joanna K.); ALSUWAIDAN (Mohammad); WOLDEYOHANNES (Hanna O.); KIM (Ashley S.); GALLAUGHER (L. Ashley) |
AF : | Department of Psychiatry, University of Toronto/Toronto, ON/Canada (1 aut.); Department of Pharmacology, University of Toronto/Toronto, ON/Canada (1 aut.); Mood Disorders Psychopharmacology Unit, University Health Network/Toronto, ON/Canada (1 aut., 2 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut.); Institute of Medical Science, University of Toronto/Toronto, ON/Canada (4 aut.); Samuel Lunenfeld Research Institute, Mount Sinai Hospital/Toronto, ON/Canada (3 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Behavioural brain research; ISSN 0166-4328; Coden BBREDI; Irlande; Da. 2013; Vol. 237; Pp. 164-171; Bibl. 66 ref. |
LA : | Anglais |
EA : | Incretins are a group of gastrointestinal hormones detected both peripherally and in the central nervous system (CNS). Recent studies have documented multiple effects of incretins on brain structure and function. Research into the neurological effects of incretins has primarily focused on animal models of neurodegenerative disorders (e.g., Alzheimer's Disease, Huntington's and Parkinson's diseases). Mood disorders (e.g. bipolar disorder (BD), major depressive disorder (MDD)) are associated with similar alterations in brain structure and function, as well as a range of cognitive deficits (e.g. memory, learning, executive function). Brain abnormalities and cognitive deficits are also found in populations with metabolic disorders (e.g., diabetes mellitus Type 2). In addition, individuals with mood disorders often have co-morbid metabolic conditions, thus treatment strategies which can effectively treat both cognitive deficits and metabolic abnormalities represent a possible integrated treatment avenue. In particular, glucagon-like peptide-1 (GLP-1 ) and its more stable, longer-lasting analogues have been demonstrated to exert neuroprotective and anti-apoptotic effects, reduce beta-amyloid (Aβ) plaque accumulation, modulate long-term potentiation and synaptic plasticity, and promote differentiation of neuronal progenitor cells. In animal models of behaviour, treatment with GLP-1 receptor agonists has been demonstrated to improve measures of cognitive function including learning and memory, as well as reduce depressive behaviour. Available GLP-1 treatments also have a favourable metabolic profile which includes weight loss and reduced risk for hypoglycemia. Systematic evaluation of the effects of GLP-1 treatment in psychiatric populations who evince cognitive deficits represents a promising treatment avenue. |
CC : | 002A26C |
FD : | Neuroprotection; Traitement; Trouble cognitif; Trouble de l'humeur; Cognition; Incrétine |
ED : | Neuroprotection; Treatment; Cognitive disorder; Mood disorder; Cognition; Incretin |
SD : | Neuroprotección; Tratamiento; Trastorno cognitivo; Trastorno humor; Cognición |
LO : | INIST-18271.354000173230240220 |
ID : | 13-0122012 |
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<front><div type="abstract" xml:lang="en">Incretins are a group of gastrointestinal hormones detected both peripherally and in the central nervous system (CNS). Recent studies have documented multiple effects of incretins on brain structure and function. Research into the neurological effects of incretins has primarily focused on animal models of neurodegenerative disorders (e.g., Alzheimer's Disease, Huntington's and Parkinson's diseases). Mood disorders (e.g. bipolar disorder (BD), major depressive disorder (MDD)) are associated with similar alterations in brain structure and function, as well as a range of cognitive deficits (e.g. memory, learning, executive function). Brain abnormalities and cognitive deficits are also found in populations with metabolic disorders (e.g., diabetes mellitus Type 2). In addition, individuals with mood disorders often have co-morbid metabolic conditions, thus treatment strategies which can effectively treat both cognitive deficits and metabolic abnormalities represent a possible integrated treatment avenue. In particular, glucagon-like peptide-1 (GLP-1 ) and its more stable, longer-lasting analogues have been demonstrated to exert neuroprotective and anti-apoptotic effects, reduce beta-amyloid (Aβ) plaque accumulation, modulate long-term potentiation and synaptic plasticity, and promote differentiation of neuronal progenitor cells. In animal models of behaviour, treatment with GLP-1 receptor agonists has been demonstrated to improve measures of cognitive function including learning and memory, as well as reduce depressive behaviour. Available GLP-1 treatments also have a favourable metabolic profile which includes weight loss and reduced risk for hypoglycemia. Systematic evaluation of the effects of GLP-1 treatment in psychiatric populations who evince cognitive deficits represents a promising treatment avenue.</div>
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<fC03 i1="02" i2="X" l="FRE"><s0>Traitement</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Treatment</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Tratamiento</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Trouble cognitif</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Cognitive disorder</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Trastorno cognitivo</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Trouble de l'humeur</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Mood disorder</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Trastorno humor</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Cognition</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Cognition</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Cognición</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Incrétine</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Incretin</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fN21><s1>098</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 13-0122012 INIST</NO>
<ET>The neuroprotective effects of GLP-1: Possible treatments for cognitive deficits in individuals with mood disorders</ET>
<AU>MCINTYRE (Roger S.); POWELL (Alissa M.); KAIDANOVICH-BEILIN (Oksana); SOCZYNSKA (Joanna K.); ALSUWAIDAN (Mohammad); WOLDEYOHANNES (Hanna O.); KIM (Ashley S.); GALLAUGHER (L. Ashley)</AU>
<AF>Department of Psychiatry, University of Toronto/Toronto, ON/Canada (1 aut.); Department of Pharmacology, University of Toronto/Toronto, ON/Canada (1 aut.); Mood Disorders Psychopharmacology Unit, University Health Network/Toronto, ON/Canada (1 aut., 2 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut.); Institute of Medical Science, University of Toronto/Toronto, ON/Canada (4 aut.); Samuel Lunenfeld Research Institute, Mount Sinai Hospital/Toronto, ON/Canada (3 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Behavioural brain research; ISSN 0166-4328; Coden BBREDI; Irlande; Da. 2013; Vol. 237; Pp. 164-171; Bibl. 66 ref.</SO>
<LA>Anglais</LA>
<EA>Incretins are a group of gastrointestinal hormones detected both peripherally and in the central nervous system (CNS). Recent studies have documented multiple effects of incretins on brain structure and function. Research into the neurological effects of incretins has primarily focused on animal models of neurodegenerative disorders (e.g., Alzheimer's Disease, Huntington's and Parkinson's diseases). Mood disorders (e.g. bipolar disorder (BD), major depressive disorder (MDD)) are associated with similar alterations in brain structure and function, as well as a range of cognitive deficits (e.g. memory, learning, executive function). Brain abnormalities and cognitive deficits are also found in populations with metabolic disorders (e.g., diabetes mellitus Type 2). In addition, individuals with mood disorders often have co-morbid metabolic conditions, thus treatment strategies which can effectively treat both cognitive deficits and metabolic abnormalities represent a possible integrated treatment avenue. In particular, glucagon-like peptide-1 (GLP-1 ) and its more stable, longer-lasting analogues have been demonstrated to exert neuroprotective and anti-apoptotic effects, reduce beta-amyloid (Aβ) plaque accumulation, modulate long-term potentiation and synaptic plasticity, and promote differentiation of neuronal progenitor cells. In animal models of behaviour, treatment with GLP-1 receptor agonists has been demonstrated to improve measures of cognitive function including learning and memory, as well as reduce depressive behaviour. Available GLP-1 treatments also have a favourable metabolic profile which includes weight loss and reduced risk for hypoglycemia. Systematic evaluation of the effects of GLP-1 treatment in psychiatric populations who evince cognitive deficits represents a promising treatment avenue.</EA>
<CC>002A26C</CC>
<FD>Neuroprotection; Traitement; Trouble cognitif; Trouble de l'humeur; Cognition; Incrétine</FD>
<ED>Neuroprotection; Treatment; Cognitive disorder; Mood disorder; Cognition; Incretin</ED>
<SD>Neuroprotección; Tratamiento; Trastorno cognitivo; Trastorno humor; Cognición</SD>
<LO>INIST-18271.354000173230240220</LO>
<ID>13-0122012</ID>
</server>
</inist>
</record>
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