Citrulline supplementation improves spatial memory in a murine model for Alzheimer’s disease

BackgroundAlzheimer’s disease (AD) correlates with the dysfunction of metabolic pathways that translates into neurological symptoms. An arginine deficiency, a precursor of nitric oxide (NO), has been reported for AD patients.ObjectiveWe aimed to evaluate the effect of citrulline oral supplementation on cognitive decline in an AD murine model.MethosThree-month citrulline or water supplementation was blindly given to male and female wild type and 3xTg-AD mice trained and tested in the Morris Water Maze (MWM). Cerebrospinal fluid and brain tissue were collected. Ultra Performance Liquid Chromatography was used for arginine determinations while the Griess method was used for NO.ResultsEight-month-old male 3xTg-AD mice supplemented with citrulline performed significantly better in the MWM task; arginine levels increased in cerebrospinal fluid although no changes were seen in brain tissue and only a tendency of increase of NO was observed.ConclusionsCitrulline oral administration is a viable treatment for memory improvement in the early stages of AD pointing to NO as a viable, efficient target for memory dysfunction in AD.

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Natriuretic Peptides in Post-mortem Brain Tissue and Cerebrospinal Fluid of Non-demented Humans and Alzheimer’s Disease Patients

Frontiers in Neuroscience ◽

10.3389/fnins.2018.00864 ◽

2018 ◽

Vol 12 ◽

Cited By ~ 1

Author(s):

Simin Mahinrad ◽

Marjolein Bulk ◽

Isabelle van der Velpen ◽

Ahmed Mahfouz ◽

Willeke van Roon-Mom ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cerebrospinal Fluid ◽

Brain Tissue ◽

Natriuretic Peptides ◽

Post Mortem ◽

Post Mortem Brain

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Telomere length and oxidative stress variations in a murine model of Alzheimer’s disease progression

10.1101/684365 ◽

2019 ◽

Author(s):

Katia Martínez-González ◽

Azul Islas-Hernández ◽

José Darío Martínez-Ezquerro ◽

Federico Bermúdez-Rattoni ◽

Paola Garcia-delaTorre

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Transgenic Mice ◽

Telomere Length ◽

Brain Tissue ◽

Murine Model ◽

Blood Cells ◽

Model Of Alzheimer’S Disease ◽

And Oxidative Stress

AbstractAlzheimer’s Disease (AD) is the most common cause of dementia and aging is its major risk factor. Changes in telomere length have been associated with aging and some degenerative diseases. Our aim was to explore some of the molecular changes caused by the progression of AD in a transgenic murine model (3xTg-AD; B6; 129-Psen1 <tm1Mpm> Tg (APPSwe, tauP301L) 1Lfa). Telomere length was assessed by qPCR in both brain tissue and peripheral blood cells and compared between three age groups: 5, 9, and 13 months. In addition, a possible effect of oxidative stress on telomere length and AD progression was explored. Shorter telomeres were found in blood cells of older transgenic mice compared to younger and wild type mice but no changes in telomere length in the hippocampus. An increase in oxidative stress with age was found for all strains but no correlation was found between oxidative stress and shorter telomere length for transgenic mice. Telomere length and oxidative stress are affected by AD progression in the 3xTg-AD murine model. Changes in blood cells are more noticeable than changes in brain tissue, suggesting that systemic changes can be detected early in the disease in this murine model.

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Cerebrospinal Fluid pH and Monoamine and Glucolytic Metabolites in Alzheimer's Disease

The British Journal of Psychiatry ◽

10.1192/bjp.124.3.280 ◽

1974 ◽

Vol 124 (580) ◽

pp. 280-287 ◽

Cited By ~ 30

Author(s):

C. G. Gottfries ◽

Åke Kjällquist ◽

Urban Pontén ◽

B. E. Roos ◽

G. Sundbärg

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cerebrospinal Fluid ◽

Brain Tissue ◽

Homovanillic Acid ◽

Monoamine Metabolites ◽

Hydroxyindoleacetic Acid ◽

The Brain ◽

Valid Information

Determinations of acid monoamine metabolites, such as homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), in cerebrospinal fluid (CSF) give valid information on the metabolism of the corresponding amines in the brain tissue (Moir et al., 1970; Roos, 1970). The monoamine metabolites in the CSF are related to age. The concentrations of HVA and 5-HIAA increase with age (Gottfries et al., 1971). Probenecid blocks the elimination of HVA and 5-HIAA from brain tissue to blood (Neff et al., 1964, 1967; Werdinius, 1966) and from CSF to blood (Guldberg et al., 1966; Olsson and Roos, 1968). Probenecid thus normally induces an increase in the concentrations of the acid monoamine metabolites in the CSF, which is related to the turnover of monoamines in the brain tissue.

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