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Article ; Online: Therapeutic Potential of Glucagon-Like Peptide-1 Cleavage Product for Alzheimer's Disease.

Day, Stephen M / Ma, Tao

2019 Volume 35, Issue 5, Page(s) 934–936

MeSH term(s)	Alzheimer Disease/drug therapy ; Animals ; Glucagon-Like Peptide 1/analogs & derivatives ; Glucagon-Like Peptide 1/physiology ; Glucagon-Like Peptide 1/therapeutic use ; Humans
Chemical Substances	glucagon-like peptide-1 (9-36)-amide ; Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2019-03-07
Publishing country	Singapore
Document type	Journal Article ; Review
ZDB-ID	2419741-5
ISSN	1995-8218 ; 1673-7067
ISSN (online)	1995-8218
ISSN	1673-7067
DOI	10.1007/s12264-019-00355-y
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Zs.A 6734: Show issues

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Article: Social inequalities in health in nonhuman primates.

Shively, Carol A / Day, Stephen M

Neurobiology of stress

2014 Volume 1, Page(s) 156–163

Abstract: Overall health has been linked to socioeconomic status, with the gap between social strata increasing each year. Studying the impact of social position on health and biological functioning in nonhuman primates has allowed researchers to model the human ... ...

Abstract	Overall health has been linked to socioeconomic status, with the gap between social strata increasing each year. Studying the impact of social position on health and biological functioning in nonhuman primates has allowed researchers to model the human condition while avoiding ethical complexities or other difficulties characteristic of human studies. Using female cynomolgus macaques (Macaca fascicularis), our lab has examined the link between social status and stress for 30 years. Female nonhuman primates are especially sensitive to social stressors which can deleteriously affect reproductive health, leading to harmful consequences to their overall health. Subordinates have lower progesterone concentrations during the luteal phase of menstrual cycle, which is indicative of absence or impairment of ovulation. Subordinate animals receive more aggression, less affiliative attention, and are more likely to exhibit depressive behaviors. They also express higher stress-related biomarkers such as increased heart rates and lower mean cortisol. While no differences in body weight between dominant and subordinate animals are observed, subordinates have lower bone density and more visceral fat than their dominant counterparts. The latter increases risk for developing inflammatory diseases. Differences are also observed in neurological and autonomic function. A growing body of data suggests that diet composition may amplify or diminish physiological stress responses which have deleterious effects on health. More experimental investigation of the health effects of diet pattern is needed to further elucidate these differences in an ongoing search to find realistic and long-term solutions to the declining health of individuals living across the ever widening socioeconomic spectrum.
Language	English
Publishing date	2014-11-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2816500-7
ISSN	2352-2895
ISSN	2352-2895
DOI	10.1016/j.ynstr.2014.11.005
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Article ; Online: Ethanol exposure alters Alzheimer's-related pathology, behavior, and metabolism in APP/PS1 mice.

Day, Stephen M / Gironda, Stephen C / Clarke, Caitlin W / Snipes, J Andy / Nicol, Noelle I / Kamran, Hana / Vaughan, Warner / Weiner, Jeffrey L / Macauley, Shannon L

Neurobiology of disease

2022 Volume 177, Page(s) 105967

Abstract: Epidemiological studies identified alcohol use disorder (AUD) as a risk factor for Alzheimer's disease (AD), yet there is conflicting evidence on how alcohol use promotes AD pathology. In this study, a 10-week moderate two-bottle choice drinking paradigm ...

Abstract	Epidemiological studies identified alcohol use disorder (AUD) as a risk factor for Alzheimer's disease (AD), yet there is conflicting evidence on how alcohol use promotes AD pathology. In this study, a 10-week moderate two-bottle choice drinking paradigm was used to identify how chronic ethanol exposure alters amyloid-β (Aβ)-related pathology, metabolism, and behavior. Ethanol-exposed APPswe/PSEN1dE9 (APP/PS1) mice showed increased brain atrophy and an increased number of amyloid plaques. Further analysis revealed that ethanol exposure led to a shift in the distribution of plaque size in the cortex and hippocampus. Ethanol-exposed mice developed a greater number of smaller plaques, potentially setting the stage for increased plaque proliferation in later life. Ethanol drinking APP/PS1 mice also exhibited deficits in nest building, a metric of self-care, as well as increased locomotor activity and central zone exploration in an open field test. Ethanol exposure also led to a diurnal shift in feeding behavior which was associated with changes in glucose homeostasis and glucose intolerance. Complementary in vivo microdialysis experiments were used to measure how acute ethanol directly modulates Aβ in the hippocampal interstitial fluid (ISF). Acute ethanol transiently increased hippocampal ISF glucose levels, suggesting that ethanol directly affects cerebral metabolism. Acute ethanol also selectively increased ISF Aβ40, but not ISF Aβ42, levels during withdrawal. Lastly, chronic ethanol drinking increased N-methyl-d-aspartate receptor (NMDAR) and decreased γ-aminobutyric acid type-A receptor (GABA
MeSH term(s)	Animals ; Mice ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloid beta-Protein Precursor/metabolism ; Disease Models, Animal ; Ethanol/toxicity ; Glucose/metabolism ; Hippocampus/metabolism ; Mice, Transgenic ; Plaque, Amyloid/metabolism ; Presenilin-1/genetics ; Presenilin-1/metabolism
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Ethanol (3K9958V90M) ; Glucose (IY9XDZ35W2) ; Presenilin-1 ; APP protein, mouse
Language	English
Publishing date	2022-12-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105967
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Zs.A 4444: Show issues

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Article: Type-2-Diabetes Alters CSF but Not Plasma Metabolomic and AD Risk Profiles in Vervet Monkeys.

Kavanagh, Kylie / Day, Stephen M / Pait, Morgan C / Mortiz, William R / Newgard, Christopher B / Ilkayeva, Olga / Mcclain, Donald A / Macauley, Shannon L

Frontiers in neuroscience

2019 Volume 13, Page(s) 843

Abstract: Epidemiological studies suggest that individuals with type 2 diabetes (T2D) have a twofold to fourfold increased risk for developing Alzheimer's disease (AD), however, the exact mechanisms linking the two diseases are unknown. In both conditions, the ... ...

Abstract	Epidemiological studies suggest that individuals with type 2 diabetes (T2D) have a twofold to fourfold increased risk for developing Alzheimer's disease (AD), however, the exact mechanisms linking the two diseases are unknown. In both conditions, the majority of pathophysiological changes, including glucose and insulin dysregulation, insulin resistance, and AD-related changes in Aβ and tau, occur decades before the onset of clinical symptoms and diagnosis. In this study, we investigated the relationship between metabolic biomarkers associated with T2D and amyloid pathology including Aβ levels, from cerebrospinal fluid (CSF) and fasting plasma of healthy, pre-diabetic (PreD), and T2D vervet monkeys (
Language	English
Publishing date	2019-08-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2019.00843
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Article ; Online: Glucagon-Like Peptide-1 Cleavage Product Improves Cognitive Function in a Mouse Model of Down Syndrome.

Day, Stephen M / Yang, Wenzhong / Wang, Xin / Stern, Jennifer E / Zhou, Xueyan / Macauley, Shannon L / Ma, Tao

eNeuro

2019 Volume 6, Issue 2

Abstract: Currently there is no effective therapy available for cognitive impairments in Down syndrome (DS), one of the most prevalent forms of intellectual disability in humans associated with the chromosomes 21 trisomy. Glucagon-like peptide-1 (GLP-1) is an ... ...

Abstract	Currently there is no effective therapy available for cognitive impairments in Down syndrome (DS), one of the most prevalent forms of intellectual disability in humans associated with the chromosomes 21 trisomy. Glucagon-like peptide-1 (GLP-1) is an incretin hormone that maintains glucose homeostasis by stimulating insulin secretion. Its natural cleavage product GLP-1 (9-36) lacks insulinotropic effects and has a low binding affinity for GLP-1 receptors; thus, GLP-1 (9-36) has historically been identified as an inactive metabolite. Conversely, recent work has demonstrated interesting physiological properties of GLP-1 (9-36) such as cardioprotection and neuroprotection. We have previously shown that GLP-1 (9-36) administration enhances neuronal plasticity in young WT mice and ameliorates cognitive deficits in a mouse model of Alzheimer's disease. Here, we report that systemic administration of GLP-1 (9-36) in Ts65Dn DS model mice of either sex resulted in decreased mitochondrial oxidative stress in hippocampus and improved dendritic spine morphology, increase of mature spines and reduction of immature spines. Importantly, these molecular alterations translated into functional changes in that long-term potentiation failure and cognitive impairments in TsDn65 DS model mice were rescued with GLP-1 (9-36) treatment. We also show that chronic GLP-1 (9-36) treatment did not alter glucose tolerance in either WT or DS model mice. Our findings suggest that GLP-1 (9-36) treatment may have therapeutic potential for DS and other neurodegenerative diseases associated with increased neuronal oxidative stress.
MeSH term(s)	Animals ; Avoidance Learning/drug effects ; Behavior, Animal/drug effects ; Cognitive Dysfunction/drug therapy ; Dendritic Spines/drug effects ; Disease Models, Animal ; Down Syndrome/drug therapy ; Female ; Glucagon-Like Peptide 1/administration & dosage ; Glucagon-Like Peptide 1/analogs & derivatives ; Glucagon-Like Peptide 1/pharmacology ; Glucose Tolerance Test ; Hippocampus/drug effects ; Long-Term Potentiation/drug effects ; Male ; Mice ; Mice, Transgenic ; Neuronal Plasticity/drug effects ; Nootropic Agents/administration & dosage ; Nootropic Agents/pharmacology ; Oxidative Stress/drug effects ; Spatial Memory/drug effects
Chemical Substances	Nootropic Agents ; glucagon-like peptide-1 (9-36)-amide ; Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2019-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0031-19.2019
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Article ; Online: A nonhuman primate model of human non-suicidal self-injury: serotonin-transporter genotype-mediated typologies.

Wood, Elizabeth K / Kruger, Ryno / Day, Jaclyn P / Day, Stephen M / Hunter, Jacob N / Neville, Leslie / Lindell, Stephen G / Barr, Christina S / Schwandt, Melanie L / Goldman, David / Suomi, Stephen J / Harris, James C / Higley, J Dee

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2021 Volume 47, Issue 6, Page(s) 1256–1262

Abstract: While non-suicidal self-injury (NSSI) occurs in the general population at a surprisingly high rate, with higher rates among certain clinical populations, its etiology is not well-understood. Consequently, the DSM-5 lists NSSI as requiring further ... ...

Abstract	While non-suicidal self-injury (NSSI) occurs in the general population at a surprisingly high rate, with higher rates among certain clinical populations, its etiology is not well-understood. Consequently, the DSM-5 lists NSSI as requiring further research. This study utilizes a translational model of naturally-occurring NSSI to assess the role of early parental neglect and variation in the serotonin transporter genotype (5-HTT) in the etiology of NSSI. Subjects (N = 161) were rhesus macaques (Macaca mulatta) reared in one of three conditions (mother-reared (MR), peer-reared (PR), or surrogate peer-reared (SPR)), and classified as NSSI (n = 18) or non-NSSI (n = 143). Subjects were genotyped for 5-HTT and their behaviors were recorded during an ecologically-meaningful, stress-evoking, intruder paradigm. Two weeks prior to testing, blood samples were obtained and assayed for plasma cortisol and adrenocorticotropic hormone (ACTH) concentrations. NSSI subjects were more likely to be SPR, paralleling human studies showing that individuals that exhibit NSSI tend to have experienced abuse or neglect early in life. Results also indicated that variation in the 5-HTT genotype differentiated the NSSI subjects. NSSI subjects that were homozygous for the L allele exhibited high plasma ACTH and high rates of stress-induced stereotypies; whereas NSSI subjects with the s allele exhibited impulsive behaviors, including frequently approaching the potentially dangerous intruder, high rates of aggressive vocal threats, and more activity. These results suggest that there may be different 5-HTT genotype-mediated NSSI typologies and that both early experiences and variation in the 5-HTT genotype may be important factors in understanding the etiology of NSSI.
MeSH term(s)	Adrenocorticotropic Hormone ; Animals ; Genotype ; Humans ; Macaca mulatta/genetics ; Self-Injurious Behavior/genetics ; Serotonin ; Serotonin Plasma Membrane Transport Proteins/genetics
Chemical Substances	Serotonin Plasma Membrane Transport Proteins ; Serotonin (333DO1RDJY) ; Adrenocorticotropic Hormone (9002-60-2)
Language	English
Publishing date	2021-04-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-021-00994-8
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Zs.A 2379: Show issues

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Article ; Online: Glucagon-like peptide-1 cleavage product GLP-1 (9-36) amide enhances hippocampal long-term synaptic plasticity in correlation with suppression of Kv4.2 expression and eEF2 phosphorylation.

Day, Stephen M / Yang, Wenzhong / Ewin, Sarah / Zhou, Xueyan / Ma, Tao

Hippocampus

2017 Volume 27, Issue 12, Page(s) 1264–1274

Abstract: Glucagon-like peptide-1 (GLP-1) is an endogenous gut hormone and a key regulator in maintaining glucose homeostasis by stimulating insulin secretion. Its natural cleavage product GLP-1 (9-36), used to be considered a "bio-inactive" metabolite mainly ... ...

Abstract	Glucagon-like peptide-1 (GLP-1) is an endogenous gut hormone and a key regulator in maintaining glucose homeostasis by stimulating insulin secretion. Its natural cleavage product GLP-1 (9-36), used to be considered a "bio-inactive" metabolite mainly because of its lack of insulinotropic effects and low affinity for GLP-1 receptors, possesses unique properties such as anti-oxidant and cardiovascular protection. Little is known about the role of GLP-1 (9-36) in central nervous system. Here we report that chronic, systemic application of GLP-1 (9-36) in adult mice facilitated both the induction and maintenance phases of hippocampal long-term potentiation (LTP), a major form of synaptic plasticity. In contrast, spatial learning and memory, as assessed by the Morris water maze test, was not altered by GLP-1 (9-36) administration. At the molecular level, GLP-1 (9-36) reduced protein levels of the potassium channel Kv4.2 in hippocampus, which is linked to elevated dendritic membrane excitability. Moreover, GLP-1(9-36) treatment inhibited phosphorylation of mRNA translational factor eEF2, which is associated with increased capacity for de novo protein synthesis. Finally, we showed that the LTP-enhancing effects by GLP-1 (9-36) treatment in vivo were blunted by application of exendin(9-39)amide [EX(9-39)], the GLP-1 receptor (GLP-1R) antagonist, suggesting its role as a GLP-1R agonist. These findings demonstrate that GLP-1 (9-36), which was considered a "bio-inactive" peptide, clearly exerts physiological effects on neuronal plasticity in the hippocampus, a brain region critical for learning and memory.
MeSH term(s)	Animals ; Blotting, Western ; Central Nervous System Agents/administration & dosage ; Female ; Glucagon-Like Peptide 1/administration & dosage ; Glucagon-Like Peptide 1/analogs & derivatives ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide-1 Receptor/antagonists & inhibitors ; Glucagon-Like Peptide-1 Receptor/metabolism ; Hippocampus/drug effects ; Hippocampus/metabolism ; Long-Term Potentiation/drug effects ; Long-Term Potentiation/physiology ; Male ; Maze Learning/drug effects ; Maze Learning/physiology ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice, Inbred C57BL ; Peptides/administration & dosage ; Peptides/metabolism ; Phosphorylation/drug effects ; Phosphorylation/physiology ; Protein-Serine-Threonine Kinases/metabolism ; Shal Potassium Channels/metabolism ; Spatial Memory/drug effects ; Spatial Memory/physiology ; Tissue Culture Techniques
Chemical Substances	Central Nervous System Agents ; Glucagon-Like Peptide-1 Receptor ; Peptides ; Shal Potassium Channels ; glucagon-like peptide-1 (9-36)-amide ; Glucagon-Like Peptide 1 (89750-14-1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; eIF2alpha kinase, mouse (EC 2.7.11.1)
Language	English
Publishing date	2017-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1074352-2
ISSN	1098-1063 ; 1050-9631
ISSN (online)	1098-1063
ISSN	1050-9631
DOI	10.1002/hipo.22795
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Zs.A 3227: Show issues

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Article ; Online: KATP channels are necessary for glucose-dependent increases in amyloid-β and Alzheimer's disease-related pathology.

JCI insight

2023 Volume 8, Issue 10

Abstract: Elevated blood glucose levels, or hyperglycemia, can increase brain excitability and amyloid-β (Aβ) release, offering a mechanistic link between type 2 diabetes and Alzheimer's disease (AD). Since the cellular mechanisms governing this relationship are ... ...

Abstract	Elevated blood glucose levels, or hyperglycemia, can increase brain excitability and amyloid-β (Aβ) release, offering a mechanistic link between type 2 diabetes and Alzheimer's disease (AD). Since the cellular mechanisms governing this relationship are poorly understood, we explored whether ATP-sensitive potassium (KATP) channels, which couple changes in energy availability with cellular excitability, play a role in AD pathogenesis. First, we demonstrate that KATP channel subunits Kir6.2/KCNJ11 and SUR1/ABCC8 were expressed on excitatory and inhibitory neurons in the human brain, and cortical expression of KCNJ11 and ABCC8 changed with AD pathology in humans and mice. Next, we explored whether eliminating neuronal KATP channel activity uncoupled the relationship between metabolism, excitability, and Aβ pathology in a potentially novel mouse model of cerebral amyloidosis and neuronal KATP channel ablation (i.e., amyloid precursor protein [APP]/PS1 Kir6.2-/- mouse). Using both acute and chronic paradigms, we demonstrate that Kir6.2-KATP channels are metabolic sensors that regulate hyperglycemia-dependent increases in interstitial fluid levels of Aβ, amyloidogenic processing of APP, and amyloid plaque formation, which may be dependent on lactate release. These studies identify a potentially new role for Kir6.2-KATP channels in AD and suggest that pharmacological manipulation of Kir6.2-KATP channels holds therapeutic promise in reducing Aβ pathology in patients with diabetes or prediabetes.
MeSH term(s)	Humans ; Mice ; Animals ; KATP Channels/metabolism ; Alzheimer Disease/pathology ; Diabetes Mellitus, Type 2/complications ; Glucose ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Hyperglycemia
Chemical Substances	KATP Channels ; Glucose (IY9XDZ35W2) ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor
Language	English
Publishing date	2023-05-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.162454
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Article: Mediterranean diet, stress resilience, and aging in nonhuman primates.

Shively, Carol A / Appt, Susan E / Chen, Haiying / Day, Stephen M / Frye, Brett M / Shaltout, Hossam A / Silverstein-Metzler, Marnie G / Snyder-Mackler, Noah / Uberseder, Beth / Vitolins, Mara Z / Register, Thomas C

Neurobiology of stress

2020 Volume 13, Page(s) 100254

Abstract: Persistent psychological stress increases the risk of many chronic diseases of aging. Little progress has been made to effectively reduce stress responses or mitigate stress effects suggesting a need for better understanding of factors that influence ... ...

Abstract	Persistent psychological stress increases the risk of many chronic diseases of aging. Little progress has been made to effectively reduce stress responses or mitigate stress effects suggesting a need for better understanding of factors that influence stress responses. Limited evidence suggests that diet may be a factor in modifying the effects of stress. However, long-term studies of diet effects on stress reactive systems are not available, and controlled randomized clinical trials are difficult and costly. Here we report the outcomes of a controlled, randomized preclinical trial of the effects of long-term consumption (31 months, ~ equivalent to 9 human years) of Western versus Mediterranean - like diets on behavioral and physiological responses to acute (brief social separation) and chronic (social subordination) psychosocial stress in 38 adult, socially-housed, female cynomolgus macaques. Compared to animals fed a Western diet, those fed the Mediterranean diet exhibited enhanced stress resilience as indicated by lower sympathetic activity, brisker and more overt heart rate responses to acute stress, more rapid recovery, and lower cortisol responses to acute psychological stress and adrenocorticotropin (ACTH) challenge. Furthermore, age-related increases in sympathetic activity and cortisol responses to stress were delayed by the Mediterranean diet. Population level diet modification in humans has been shown to be feasible. Our findings suggest that population-wide adoption of a Mediterranean-like diet pattern may provide a cost-effective intervention on psychological stress and promote healthy aging with the potential for widespread efficacy.
Language	English
Publishing date	2020-10-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2816500-7
ISSN	2352-2895
ISSN	2352-2895
DOI	10.1016/j.ynstr.2020.100254
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