Characterization of Cerebrospinal Fluid (CSF) and Plasma NPY Levels in Normal Volunteers over a 24-h Timeframe

Baker, Dewleen G.; Hauger, Richard L.; Bertram, Tobias Moeller; Patel, Piyush M.; Barkauskas, Donald A.; Clopton, Paul; Geracioti, Thomas D.; O’Connor, Daniel T.; Nievergelt, Caroline M.

doi:10.1016/b978-0-12-800044-1.00199-9

Cited by 6 publications

(8 citation statements)

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“…In our analysis, the source of NPY (CSF vs. plasma) was not associated with changes in SMDs (effect size, see Supporting Information 3, Table ). This suggests that changes in the NPY levels in plasma or CSF are likely proportional, in agreement with Baker and colleagues (). It is simply that in our data CSF NPY levels in MDD did not achieve statistical significance.…”

Section: Discussionsupporting

confidence: 90%

“…Previous studies have reported that NPY levels in CSF are approximately two to threefold higher than in plasma (Baker et al, ; Dötsch et al, ). The ratio is constant over 24 hr, and is independent of changes in personal or physiological parameters (Baker et al, ). In our analysis, the source of NPY (CSF vs. plasma) was not associated with changes in SMDs (effect size, see Supporting Information 3, Table ).…”

Section: Discussionmentioning

confidence: 93%

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Neuropeptide Y in PTSD, MDD, and chronic stress: A systematic review and meta‐analysis

Tural

Iosifescu

2020

J of Neuroscience Research

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Previous studies have suggested that neuropeptide Y (NPY) levels may be altered in patients with major depressive disorder (MDD), post‐traumatic stress disorder (PTSD) and chronic stress. We investigated, through systematic review and meta‐analysis, whether the mean levels of NPY are significantly different in patients with MDD, PTSD or chronic stress, compared to controls. The main outcome was the pooled standardized mean difference (SMD) with 95% confidence intervals between cases and controls, using the random‐effects model. Heterogeneity and publication bias were evaluated. Thirty‐five studies met eligibility criteria. Meta‐regression determined that medication and sex could explain 27% of the between‐study variance. Females and participants currently prescribed psychotropic medications had significantly higher levels of NPY. NPY levels were significantly lower in plasma and cerebrospinal fluid (CSF) in PTSD patients versus controls. Patients with MDD had significantly lower levels of NPY in plasma compared to controls, but not in the CSF. The magnitudes of the decrease in plasma NPY levels were not significantly different between PTSD and MDD. However, chronic stress patients had significantly higher plasma NPY levels compared to controls, PTSD or MDD. Our findings may imply a shared role of NPY in trauma and depression: nevertheless, it is not clear that the association is specific to these disorders. Psychotropic medications may help restore NPY levels. Further controlled studies are needed to better delineate the contribution of confounding variables such as type of depression, body mass index, appetite or sleep architecture.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 93%

Neuropeptide Y in PTSD, MDD, and chronic stress: A systematic review and meta‐analysis

Tural

Iosifescu

2020

J of Neuroscience Research

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“…NPY is also found in the peripheral nervous system and adrenal gland . As adrenalectomy does not significantly affect peripheral NPY levels and there is some correlation between CSF NPY levels and plasma NPY levels, it is thought that peripheral NPY levels have a neural origin. To date, changes in the peripheral NPY levels across the ALS‐FTD were unknown.…”

Section: Discussionmentioning

confidence: 99%

Eating peptides: biomarkers of neurodegeneration in amyotrophic lateral sclerosis and frontotemporal dementia

Ahmed

Phan

Highton‐Williamson

et al. 2019

Ann Clin Transl Neurol

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Objective Physiological changes potentially influence disease progression and survival along the Amyotrophic Lateral Sclerosis (ALS)‐Frontotemporal dementia (FTD) spectrum. The peripheral peptides that regulate eating and metabolism may provide diagnostic, metabolic, and progression biomarkers. The current study aimed to examine the relationships and biomarker potential of hormonal peptides. Methods One hundred and twenty‐seven participants (36 ALS, 26 ALS‐ cognitive, patients with additional cognitive behavioral features, and 35 behavioral variant FTD (bvFTD) and 30 controls) underwent fasting blood analyses of leptin, ghrelin, neuropeptide Y (NPY), peptide YY (PYY), and insulin levels. Relationships between endocrine measures, cognition, eating behaviors, and body mass index (BMI) were investigated. Biomarker potential was evaluated using multinomial logistic regression for diagnosis and correlation to disease duration. Results Compared to controls, ALS and ALS‐cognitive had higher NPY levels and bvFTD had lower NPY levels, while leptin levels were increased in all patient groups. All groups had increased insulin levels and a state of insulin resistance compared to controls. Lower NPY levels correlated with increasing eating behavioral change and BMI, while leptin levels correlated with BMI. On multinomial logistic regression, NPY and leptin levels were found to differentiate between diagnosis. Reduced Neuropeptide Y levels correlated with increasing disease duration, suggesting it may be useful as a potential marker of disease progression. Interpretation ALS‐FTD is characterized by changes in NPY and leptin levels that may impact on the underlying regional neurodegeneration as they were predictive of diagnosis and disease duration, offering the potential as biomarkers and for the development of interventional treatments.

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“…Similarly, after exposing healthy subjects to uncontrollable stress, NPY plasma levels increased together with cortisol and noradrenaline (Morgan et al, 2001;Rasmusson et al, 2010). As mentioned above, plasma NPY mainly serves as an indicator for sympathetic activity and correlations between plasma and CSF concentrations are also relatively weak (Baker et al, 2013). NPY in the plasma may, however, also interact with Y receptors in brain areas that are partially open to the blood-brain barrier, such as the arcuate nucleus of the hypothalamus or the area postrema.…”

Section: Response Of Npy Plasma Levels To Sympathetic Stimulation Stmentioning

confidence: 90%

The role of Neuropeptide Y in fear conditioning and extinction

et al. 2016

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While anxiety disorders are the brain disorders with the highest prevalence and constitute a major burden for society, a considerable number of affected people are still treated insufficiently. Thus, in an attempt to identify potential new anxiolytic drug targets, neuropeptides have gained considerable attention in recent years. Compared to classical neurotransmitters they often have a regionally restricted distribution and may bind to several distinct receptor subtypes. Neuropeptide Y (NPY) is a highly conserved neuropeptide that is specifically concentrated in limbic brain areas and signals via at least 5 different G-protein-coupled receptors. It is involved in a variety of physiological processes including the modulation of emotional-affective behaviors. An anxiolytic and stress-reducing property of NPY is supported by many preclinical studies. Whether NPY may also interact with processing of learned fear and fear extinction is comparatively unknown. However, this has considerable relevance since pathological, inappropriate and generalized fear expression and impaired fear extinction are hallmarks of human post-traumatic stress disorder and a major reason for its treatment-resistance. Recent evidence from different laboratories emphasizes a fear-reducing role of NPY, predominantly mediated by exogenous NPY acting on Y1 receptors. Since a reduction of fear expression was also observed in Y1 receptor knockout mice, other Y receptors may be equally important. By acting on Y2 receptors, NPY promotes fear extinction and generates a long-term suppression of fear, two important preconditions that could support cognitive behavioral therapies in human patients. A similar effect has been demonstrated for the closely related pancreatic polypeptide (PP) when acting on Y4 receptors. Preliminary evidence suggests that NPY modulates fear in particular by activation of Y1 and Y2 receptors in the basolateral and central amygdala, respectively. In the basolateral amygdala, NPY signaling activates inhibitory G protein-coupled inwardly-rectifying potassium channels or suppresses hyperpolarization-induced I(h) currents in a Y1 receptor-dependent fashion, favoring a general suppression of neuronal activity. A more complex situation has been described for the central extended amygdala, where NPY reduces the frequency of inhibitory and excitatory postsynaptic currents. In particular the inhibition of long-range central amygdala output neurons may result in a Y2 receptor-dependent suppression of fear. The role of NPY in processes of learned fear and fear extinction is, however, only beginning to emerge, and multiple questions regarding the relevance of endogenous NPY and different receptor subtypes remain elusive. Y2 receptors may be of particular interest for future studies, since they are the most prominent Y receptor subtype in the human brain and thus among the most promising therapeutic drug targets when translating preclinical evidence to potential new therapies for human anxiety disorders.

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Characterization of Cerebrospinal Fluid (CSF) and Plasma NPY Levels in Normal Volunteers over a 24-h Timeframe

Cited by 6 publications

References 0 publications

Neuropeptide Y in PTSD, MDD, and chronic stress: A systematic review and meta‐analysis

Neuropeptide Y in PTSD, MDD, and chronic stress: A systematic review and meta‐analysis

Eating peptides: biomarkers of neurodegeneration in amyotrophic lateral sclerosis and frontotemporal dementia

The role of Neuropeptide Y in fear conditioning and extinction

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