Age‐related cognitive impairment is associated with low serum concentrations of testosterone and CSF levels of amyloid beta 42 in male cynomolgus monkeys ( Macaca fascicularis )

2021 ◽  
Vol 50 (5) ◽  
pp. 270-272
Author(s):  
Huda Shalahudin Darusman ◽  
Tan Li Wern ◽  
Dondin Sajuthi ◽  
Steven J. Schapiro ◽  
Jann Hau
Keyword(s):  
Cognitive Impairment ◽  
Amyloid Beta ◽  
Macaca Fascicularis ◽  
Serum Concentrations ◽  
Cynomolgus Monkeys ◽  
Age Related ◽  
Csf Levels ◽  
Amyloid Beta 42 ◽  
Low Serum

Suppression of spermatogenesis in a nonhuman primate (Macaca fascicularis) by concomitant gonadotropin-releasing hormone antagonist and testosterone treatment

1987 ◽  
Vol 114 (1) ◽  
pp. 138-146 ◽  
Author(s):  
G. F. Weinbauer ◽  
F. J. Surmann ◽  
E. Nieschlag
Keyword(s):  
Macaca Fascicularis ◽  
Gnrh Antagonist ◽  
Gonadotropin Releasing Hormone ◽  
Serum Concentrations ◽  
Sperm Production ◽  
Cynomolgus Monkeys ◽  
Releasing Hormone ◽  
Testicular Regression ◽  
Pre Treatment ◽  
Testicular Histology

Abstract. The effects of concomitant testosterone (T)-supplementation on gonadotropin-releasing hormone (GnRH) antagonist-induced testicular regression in cynomolgus monkeys (M. fascicularis) were investigated. Four adult monkeys were infused via osmotic minipumps with daily amounts of 2 mg of a potent GnRH antagonist (N-Ac-D-Nal(2)1, D-pCl-Phe2, D-Trp3, D-hArg (Et2)6, D-Ala10)-GnRH (RS-68439) for a period of 104 days. Androgen substitution was provided via T-filled Silastic capsules implanted at initiation of GnRH antagonist treatment. Within 1–4 days of GnRH antagonist administration, serum concentrations of bioactive LH became undetectable. The implants maintained serum T at 50–80% of pre-treatment levels. Sperm production decreased in three out of four monkeys. One animal became azoospermic by the 13th week of treatment and the ejaculates of two other monkeys contained less than 5 × 106 sperm. In the fourth monkey, spermatogenesis was less affected. Testicular histology, judging from biopsies at termination of GnRH antagonist treatment, was typical of the hypogonadotropic status in 3 of the 4 monkeys. The most affected tubules contained only spermatogonia and Sertoli cells. Although comparison with GnRH antagonist treatment alone in a previous study indicated a delay of spermatogenic inhibition with testosterone, the present study confirms the potential of GnRH antagonist for male fertility regulation.

scholarly journals Amyloid beta-42 Levels in Companion Dog Brains Correlate with Age and Cognitive Function

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 887-887
Author(s):  
Silvan Urfer ◽  
Martin Darvas ◽  
Dirk Keene ◽  
Kálman Czeibert ◽  
Enikő Kubinyi ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Cognitive Dysfunction ◽  
Amyloid Beta ◽  
Temporal Cortex ◽  
Brain Regions ◽  
Aging Research ◽  
Human Environment ◽  
Luminex Assay ◽  
Age Related ◽  
Amyloid Beta 42

Abstract The privately owned companion dog is an increasingly important model in aging research because it shares the human environment, is exposed to similar environmental risk factors, receives comparable medical care, and develops many of the same age-related pathologies. One such pathology is Canine Cognitive Dysfunction (CCD), which shares many of the clinical features of human Alzheimer’s Disease (AD), including progressive loss of cognitive function, loss of normal sleep patterns, increased anxiety, and aimless wandering. Amyloid-beta 42 (Aβ42) plaques similar to these found in humans with AD are known to naturally occur in the brains of aged dogs, making them an intriguing potential model for AD in humans. As part of the Dog Aging Project (www.dogagingproject.org), we studied frozen samples taken from the frontal cortex, medial temporal cortex, entorhinal cortex, and hippocampus of n=24 companion dogs of various ages that were euthanized for unrelated health reasons and donated by their owners. Brains were removed and frozen within 4 hours post mortem. Using a novel quantitative Luminex assay, we found a significant correlation between age and Aβ42 levels in all of these brain regions, as well as a significant correlation between Aβ42 levels and cognitive function scores as measured by the Canine Cognitive Dysfunction Scale. We will now investigate histopathology in the same dogs and brain regions, and investigate whether we can also measure Tau and pTau in these samples using Luminex and mass spectrometry.

Elevated Inflammatory Markers and Arterial Stiffening Exacerbate Tau but Not Amyloid Pathology in Older Adults with Mild Cognitive Impairment

2021 ◽  
pp. 1-13
Author(s):  
Alexandra L. Clark ◽  
Alexandra J. Weigand ◽  
Kelsey R. Thomas ◽  
Seraphina K. Solders ◽  
Lisa Delano-Wood ◽  
...  
Keyword(s):  
Older Adults ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Inflammatory Markers ◽  
Memory Performance ◽  
Cognitive Testing ◽  
Interactive Effects ◽  
Protein Biomarkers ◽  
Age Related ◽  
T Tau

Background: Age-related cerebrovascular and neuroinflammatory processes have been independently identified as key mechanisms of Alzheimer’s disease (AD), although their interactive effects have yet to be fully examined. Objective: The current study examined 1) the influence of pulse pressure (PP) and inflammatory markers on AD protein levels and 2) links between protein biomarkers and cognitive function in older adults with and without mild cognitive impairment (MCI). Methods: This study included 218 ADNI (81 cognitively normal [CN], 137 MCI) participants who underwent lumbar punctures, apolipoprotein E (APOE) genotyping, and cognitive testing. Cerebrospinal (CSF) levels of eight pro-inflammatory markers were used to create an inflammation composite, and amyloid-beta 1–42 (Aβ 42), phosphorylated tau (p-tau), and total tau (t-tau) were quantified. Results: Multiple regression analyses controlling for age, education, and APOE ɛ4 genotype revealed significant PP x inflammation interactions for t-tau (B = 0.88, p = 0.01) and p-tau (B = 0.84, p = 0.02); higher inflammation was associated with higher levels of tau within the MCI group. However, within the CN group, analyses revealed a significant PP x inflammation interaction for Aβ 42 (B = –1.01, p = 0.02); greater inflammation was associated with higher levels of Aβ 42 (indicative of lower cerebral amyloid burden) in those with lower PP. Finally, higher levels of tau were associated with poorer memory performance within the MCI group only (p s <  0.05). Conclusion: PP and inflammation exert differential effects on AD CSF proteins and provide evidence that vascular risk is associated with greater AD pathology across our sample of CN and MCI older adults.

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