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Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice. / Gengler, Simon; McClean, Paula L.; McCurtin, Ruth et al.
In: Neurobiology of Aging, Vol. 33, No. 2, 02.2012, p. 265-276.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Gengler, S, McClean, PL, McCurtin, R, Gault, VA & Holscher, C 2012, 'Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice', Neurobiology of Aging, vol. 33, no. 2, pp. 265-276. https://doi.org/10.1016/j.neurobiolaging.2010.02.014

APA

Gengler, S., McClean, P. L., McCurtin, R., Gault, V. A., & Holscher, C. (2012). Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice. Neurobiology of Aging, 33(2), 265-276. https://doi.org/10.1016/j.neurobiolaging.2010.02.014

Vancouver

Gengler S, McClean PL, McCurtin R, Gault VA, Holscher C. Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice. Neurobiology of Aging. 2012 Feb;33(2):265-276. doi: 10.1016/j.neurobiolaging.2010.02.014

Author

Gengler, Simon ; McClean, Paula L. ; McCurtin, Ruth et al. / Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice. In: Neurobiology of Aging. 2012 ; Vol. 33, No. 2. pp. 265-276.

Bibtex

@article{76080623a80542a89e5ff91eaf0c8d15,
title = "Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice",
abstract = "Diabetes is a risk factor for Alzheimer's disease. We tested the effects of Val(8)GLP-1, an enzyme-resistant analogue of the incretin hormone glucagon-like peptide 1 originally developed to treat diabetes in a mouse model of Alzheimer's disease that expresses mutated amyloid precursor protein (APP) and presenilin-1. We tested long term potentiation (LTP) of synaptic plasticity, inflammation response, and plaque formation. Val(8)GLP-1 crosses the blood-brain barrier when administered via intraperitoneal injection. Val(8)GLP-1 protected LTP in 9- and 18-month-old Alzheimer's disease mice when given for 3 weeks at 25 nmol/kg intraperitoneally. LTP was also enhanced in 18-month-old wild type mice, indicating that Val(8)GLP-1 also ameliorates age-related synaptic degenerative processes. Paired-pulse facilitation was also enhanced. The number of beta-amyloid plaques and microglia activation in the cortex increased with age but was not reduced by Val(8)GLP-1. In 18-month-old mice, however, the number of Congo red positive dense-core amyloid plaques was reduced. Treatment with Val(8)GLP-1 might prevent or delay neurodegenerative processes.",
keywords = "Blood-brain barrier, Brain , Diabetes , Insulin signaling , Neurons , Neuropeptide , Synaptic plasticity",
author = "Simon Gengler and McClean, {Paula L.} and Ruth McCurtin and Gault, {Victor A.} and Christian Holscher",
year = "2012",
month = feb,
doi = "10.1016/j.neurobiolaging.2010.02.014",
language = "English",
volume = "33",
pages = "265--276",
journal = "Neurobiology of Aging",
issn = "0197-4580",
publisher = "Elsevier Inc.",
number = "2",

}

RIS

TY - JOUR

T1 - Val(8)GLP-1 rescues synaptic plasticity and reduces dense core plaques in APP/PS1 mice

AU - Gengler, Simon

AU - McClean, Paula L.

AU - McCurtin, Ruth

AU - Gault, Victor A.

AU - Holscher, Christian

PY - 2012/2

Y1 - 2012/2

N2 - Diabetes is a risk factor for Alzheimer's disease. We tested the effects of Val(8)GLP-1, an enzyme-resistant analogue of the incretin hormone glucagon-like peptide 1 originally developed to treat diabetes in a mouse model of Alzheimer's disease that expresses mutated amyloid precursor protein (APP) and presenilin-1. We tested long term potentiation (LTP) of synaptic plasticity, inflammation response, and plaque formation. Val(8)GLP-1 crosses the blood-brain barrier when administered via intraperitoneal injection. Val(8)GLP-1 protected LTP in 9- and 18-month-old Alzheimer's disease mice when given for 3 weeks at 25 nmol/kg intraperitoneally. LTP was also enhanced in 18-month-old wild type mice, indicating that Val(8)GLP-1 also ameliorates age-related synaptic degenerative processes. Paired-pulse facilitation was also enhanced. The number of beta-amyloid plaques and microglia activation in the cortex increased with age but was not reduced by Val(8)GLP-1. In 18-month-old mice, however, the number of Congo red positive dense-core amyloid plaques was reduced. Treatment with Val(8)GLP-1 might prevent or delay neurodegenerative processes.

AB - Diabetes is a risk factor for Alzheimer's disease. We tested the effects of Val(8)GLP-1, an enzyme-resistant analogue of the incretin hormone glucagon-like peptide 1 originally developed to treat diabetes in a mouse model of Alzheimer's disease that expresses mutated amyloid precursor protein (APP) and presenilin-1. We tested long term potentiation (LTP) of synaptic plasticity, inflammation response, and plaque formation. Val(8)GLP-1 crosses the blood-brain barrier when administered via intraperitoneal injection. Val(8)GLP-1 protected LTP in 9- and 18-month-old Alzheimer's disease mice when given for 3 weeks at 25 nmol/kg intraperitoneally. LTP was also enhanced in 18-month-old wild type mice, indicating that Val(8)GLP-1 also ameliorates age-related synaptic degenerative processes. Paired-pulse facilitation was also enhanced. The number of beta-amyloid plaques and microglia activation in the cortex increased with age but was not reduced by Val(8)GLP-1. In 18-month-old mice, however, the number of Congo red positive dense-core amyloid plaques was reduced. Treatment with Val(8)GLP-1 might prevent or delay neurodegenerative processes.

KW - Blood-brain barrier

KW - Brain

KW - Diabetes

KW - Insulin signaling

KW - Neurons

KW - Neuropeptide

KW - Synaptic plasticity

UR - http://www.scopus.com/inward/record.url?scp=82755176046&partnerID=8YFLogxK

U2 - 10.1016/j.neurobiolaging.2010.02.014

DO - 10.1016/j.neurobiolaging.2010.02.014

M3 - Journal article

AN - SCOPUS:82755176046

VL - 33

SP - 265

EP - 276

JO - Neurobiology of Aging

JF - Neurobiology of Aging

SN - 0197-4580

IS - 2

ER -