scholarly journals Age-related reduction in frequency-following responses as a potential marker of cochlear neural degeneration

2021 ◽  
pp. 108411
Author(s):  
Jonatan Märcher-Rørsted ◽  
Gerard Encina-Llamas ◽  
Torsten Dau ◽  
M. Charles Liberman ◽  
Pei-zhe Wu ◽  
...  
Keyword(s):  
Neural Degeneration ◽  
Age Related ◽  
Potential Marker

Age-related neural degeneration in nuclear-factor κB p50 knockout mice

Neuroscience ◽  
2006 ◽  
Vol 139 (3) ◽  
pp. 965-978 ◽  
Author(s):  
Z.-Y. Lu ◽  
S.P. Yu ◽  
J.-F. Wei ◽  
L. Wei
Keyword(s):  
Knockout Mice ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Neural Degeneration ◽  
Age Related

scholarly journals Investigating the Relationship between Diabetes and Alzheimer’s Disease:

2020 ◽  
Vol 7 (1) ◽  
pp. 1-11
Author(s):  
Tammanna R. Sahrawat ◽  
Jyoti Dwivedi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
System Biology ◽  
Network System ◽  
System Biology Approach ◽  
Common Elements ◽  
Age Related ◽  
Potential Marker ◽  
The Common ◽  
The Relationship

Ageing is associated with a number of diseases. Alzheimer’s disease (AD) and diabetes are among such most common diseases. These two diseases are considered to be fundamentally similar disorders because they share some common elements, though they differ in the time of onset, tissues affected as well as the magnitudes of their specific traits. The present study was undertaken to prospect the association between the genes involved in Diabetes and AD; and their common pathophysiology. Using a network system biology approach, the genes common between Diabetes and AD were retrieved from DisGeNET database. The common genes were analysed using in silico tool, Cyctoscape’s various plug-ins, ClusterONE, CytoHubba, ClueGO and CluePedia. Eleven genes which can act as potential marker for both Diabetes and AD namely IL4, ICAM1, ALB, INS, CSF2, IL6, TNF, IL10, GAPDH, TLR4, and AKT have been identified in the present study. This is the first study of its kind in which relationship between Diabetes and AD has been investigated to identify their common genes, which can help in better understanding of pathophysiology of these age-related diseases.

scholarly journals Nutritional Factors Modulating Alu Methylation in an Italian Sample from The Mark-Age Study Including Offspring of Healthy Nonagenarians

Nutrients ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2986
Author(s):  
Robertina Giacconi ◽  
Marco Malavolta ◽  
Alexander Bürkle ◽  
María Moreno-Villanueva ◽  
Claudio Franceschi ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Preliminary Investigation ◽  
Methylation Status ◽  
Dietary Factors ◽  
Elderly Subjects ◽  
Nutritional Factors ◽  
Age Related ◽  
Potential Marker ◽  
Plasma Copper ◽  
Risk Of Disease

Alu hypomethylation promotes genomic instability and is associated with aging and age-related diseases. Dietary factors affect global DNA methylation, leading to changes in genomic stability and gene expression with an impact on longevity and the risk of disease. This preliminary study aims to investigate the relationship between nutritional factors, such as circulating trace elements, lipids and antioxidants, and Alu methylation in elderly subjects and offspring of healthy nonagenarians. Alu DNA methylation was analyzed in sixty RASIG (randomly recruited age-stratified individuals from the general population) and thirty-two GO (GeHA offspring) enrolled in Italy in the framework of the MARK-AGE project. Factor analysis revealed a different clustering between Alu CpG1 and the other CpG sites. RASIG over 65 years showed lower Alu CpG1 methylation than those of GO subjects in the same age class. Moreover, Alu CpG1 methylation was associated with fruit and whole-grain bread consumption, LDL2-Cholesterol and plasma copper. The preserved Alu methylation status in GO, suggests Alu epigenetic changes as a potential marker of aging. Our preliminary investigation shows that Alu methylation may be affected by food rich in fibers and antioxidants, or circulating LDL subfractions and plasma copper.

scholarly journals SUN-021 Age-Specific Multiples of the Median Level of Serum Anti-Mullerian Hormone Is a Potential Marker for Diagnosis of Polycystic Ovary Syndrome

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Hang Wun Raymond Li ◽  
Yi-Lei He ◽  
Rong Li ◽  
Ching Yin Grace Wong ◽  
Barre Sy ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Age Groups ◽  
Fertility Treatment ◽  
Reference Ranges ◽  
Ovary Syndrome ◽  
Diagnostic Threshold ◽  
Age Related ◽  
Potential Marker ◽  
Significant Difference

Abstract Serum anti-Mullerian hormone (AMH) levels are significantly higher in women with polycystic ovary syndrome (PCOS) than in normal ovulatory women. Different diagnostic cut-off values of AMH for discriminating women with PCOS from normal controls have been proposed. This is attributed partly to the different assay methods used with different calibration, as well as the age-related changes in serum AMH levels. We propose that it may be more appropriate to use age-specific multiples of the median (MoM) of AMH value instead of a “one for all ages” cut-off as a diagnostic threshold. Hence, we conducted a retrospective study to validate the performance of age-specific MoM of AMH value in the diagnosis of PCOS. We studied on a cohort of 751 women presented to the clinic for menstrual disorders or fertility treatment, including 473 women diagnosed with polycystic ovary syndrome by the Rotterdam criteria and 278 normal ovulatory controls. Their archived serum samples, collected at the early follicular phase, were retrieved and assayed for AMH by the automated Access AMH assay. The MOM AMH of each subject was calculated based on the age-specific reference ranges recently established by our group. Our results showed that MOM AMH was significantly higher in women with PCOS compared to controls (p<0.0001). When stratified into five-yearly age groups, there was no significant difference in MOM AMH (p>0.05) among women with PCOS aged 21-25, 26-30 and 31-35 years, but those aged 36-40 years had significantly higher MOM AMH (p<0.05) compared to the other younger age groups. Among the ovulatory controls, no significant difference was observed in MOM AMH among all the age groups (p>0.05). The area under the receiver-operator characteristic curve was 0.852 (95% CI 0.825-0.877) (p<0.0001) for discriminating women with PCOS from ovulatory controls by MOM AMH. The best cut-off value of MOM AMH was 1.44, and the corresponding sensitivity and specificity were 76% and 79% respectively. At the fixed specificity of 80% and the corresponding sensitivity of 73% (with positive and negative likelihood ratios of 3.8 and 0.33 respectively), the cut-off value of MOM AMH was 1.5. In conclusion, age-specific MOM AMH is a promising surrogate of antral follicle count in the diagnosis of PCOS.

scholarly journals Lack of exercise leads to significant and reversible loss of scale invariance in both aged and young mice

2015 ◽  
Vol 112 (8) ◽  
pp. 2320-2324 ◽  
Author(s):  
Changgui Gu ◽  
Claudia P. Coomans ◽  
Kun Hu ◽  
Frank A. J. L. Scheer ◽  
H. Eugene Stanley ◽  
...  
Keyword(s):  
Scale Invariance ◽  
Age Groups ◽  
Active Phase ◽  
Behavioral Activity ◽  
Scale Invariant ◽  
Healthy Humans ◽  
Age Related ◽  
Potential Marker ◽  
Lack Of Exercise ◽  
Running Wheels

In healthy humans and other animals, behavioral activity exhibits scale invariance over multiple timescales from minutes to 24 h, whereas in aging or diseased conditions, scale invariance is usually reduced significantly. Accordingly, scale invariance can be a potential marker for health. Given compelling indications that exercise is beneficial for mental and physical health, we tested to what extent a lack of exercise affects scale invariance in young and aged animals. We studied six or more mice in each of four age groups (0.5, 1, 1.5, and 2 y) and observed an age-related deterioration of scale invariance in activity fluctuations. We found that limiting the amount of exercise, by removing the running wheels, leads to loss of scale-invariant properties in all age groups. Remarkably, in both young and old animals a lack of exercise reduced the scale invariance in activity fluctuations to the same level. We next showed that scale invariance can be restored by returning the running wheels. Exercise during the active period also improved scale invariance during the resting period, suggesting that activity during the active phase may also be beneficial for the resting phase. Finally, our data showed that exercise had a stronger influence on scale invariance than the effect of age. The data suggest that exercise is beneficial as revealed by scale-invariant parameters and that, even in young animals, a lack of exercise leads to strong deterioration in these parameters.

Neural Degeneration in the Spiral Ganglia of C57BL/6 Mice

1988 ◽  
Vol 46 ◽  
pp. 136-137
Author(s):  
Glenn M. Cohen ◽  
Joseph S. Grasso
Keyword(s):  
Osmium Tetroxide ◽  
Initial Study ◽  
Uranyl Acetate ◽  
Lead Citrate ◽  
Thin Sections ◽  
Neural Degeneration ◽  
Age Related ◽  
Sensory Hair Cell ◽  
Spiral Ganglia ◽  
Old Mice

C57BL/6 mice, along with several other mouse genotypes, have served as models for human presbycusis (age-related hearing losses). C57BL/6 mice and their genetic substrain C57/bl6 show progressively severe hearing losses, starting as early as 30 days postnatally. The hearing losses result from sweeping sensory (hair cell) and neural degeneration that begins in the basal end and advances apically. For the initial study of the spiral ganglia C57BL/6 mice, our two objectives were to develop criteria for identifying the different degenerative stages and determine Whether the same degenerative stages repeat themselves in both young and old mice.Female C57BL/6 mice of seven ages, ranging from 1 1/2 to 32 months, were examined. The ears were exposed to the fixative (3.5% glutaraldehyde [GA]) within cne min after sacrifice. The cochleae were decalcified in 5% EDTA in 3.5% GA, postfixed in 1% osmium tetroxide, and embedded in Araldite 502 epoxy. Semithin (1μ) sections were stained with toluidine blue or p-phenylenediamine; thin sections were stained with uranyl acetate and lead citrate.

scholarly journals Cortical pencil lining on SWI MRI in NBIA and healthy aging

BMC Neurology ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Marlous C. M. van der Weijden ◽  
Peter Jan van Laar ◽  
Roald A. Lambrechts ◽  
Dineke S. Verbeek ◽  
Marina A. J. Tijssen
Keyword(s):  
Globus Pallidus ◽  
Healthy Subjects ◽  
Healthy Aging ◽  
Red Nucleus ◽  
Iron Accumulation ◽  
Specific Marker ◽  
Age Related ◽  
Potential Marker ◽  
Age Dependent ◽  
Subcortical Nuclei

Abstract Background Neurodegeneration with brain iron accumulation (NBIA) is characterized by pathological iron accumulation in the subcortical nuclei and the cortex. As age-related iron accumulation studies in these structures are lacking in healthy aging, we aimed to characterize the dynamics of age-dependent iron accumulation in subcortical nuclei in healthy aging and selected NBIA cases. This is fundamental to understand the natural age-related iron deposition in the healthy brain prior to using this marker as a potential prognostic or diagnostic tool in neurodegenerative disorders. Methods Susceptibility-weighted imaging (SWI) scans from 81 healthy volunteers (0-79 years) and four genetically confirmed patients suffering from NBIA (2-14 years) were obtained. We scored the presence or absence of pencil lining of the motor cortex and putamen and analyzed the normalized SWI signal intensity ratio (NSIR) in five subcortical nuclei. Results In healthy subjects, an age-dependent increase of pencil lining occurred starting from the second decade of life and was present in all cases at the age of 50. In their first decade, NBIA patients showed no cortical pencil lining, but we did observe putaminal pencil lining at this stage. In healthy subjects, age and NSIR of all nuclei correlated positively and was particularly dynamic in early childhood until young adulthood in the globus pallidus, dentate nucleus and red nucleus, but not in the caudate nucleus and putamen. NBIA patients showed an increased NSIR in the globus pallidus only and not in the other subcortical nuclei compared to age-matched healthy subjects. Conclusions Cortical pencil lining is part of healthy aging. This should be considered when assessing this as a potential marker in NBIA diagnosis and prognosis. Putaminal pencil lining has the potential to become a specific marker for some subtypes of NBIA in the first decade of life, as it was only observed in NBIA and not in age-matched healthy subjects. NSIR in the subcortical nuclei during healthy aging was shown to be dynamic, accentuating the importance of having an age-dependent baseline.

scholarly journals Serine Phosphorylation of IRS1 Correlates with Aβ-Unrelated Memory Deficits and Elevation in Aβ Level Prior to the Onset of Memory Decline in AD

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1942 ◽  
Author(s):  
Wei Wang ◽  
Daisuke Tanokashira ◽  
Yusuke Fukui ◽  
Megumi Maruyama ◽  
Chiemi Kuroiwa ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Animal Models ◽  
Biological Effects ◽  
Amyloid Β ◽  
Memory Deficits ◽  
Serine Phosphorylation ◽  
Memory Decline ◽  
Age Related ◽  
Potential Marker

The biological effects of insulin signaling are regulated by the phosphorylation of insulin receptor substrate 1 (IRS1) at serine (Ser) residues. In the brain, phosphorylation of IRS1 at specific Ser sites increases in patients with Alzheimer’s disease (AD) and its animal models. However, whether the activation of Ser sites on neural IRS1 is related to any type of memory decline remains unclear. Here, we show the modifications of IRS1 through its phosphorylation at etiology-specific Ser sites in various animal models of memory decline, such as diabetic, aged, and amyloid precursor protein (APP) knock-in NL-G-F (APPKINL-G-F) mice. Substantial phosphorylation of IRS1 at specific Ser sites occurs in type 2 diabetes- or age-related memory deficits independently of amyloid-β (Aβ). Furthermore, we present the first evidence that, in APPKINL-G-F mice showing Aβ42 elevation, the increased phosphorylation of IRS1 at multiple Ser sites occurs without memory impairment. Our findings suggest that the phosphorylation of IRS1 at specific Ser sites is a potential marker of Aβ-unrelated memory deficits caused by type 2 diabetes and aging; however, in Aβ-related memory decline, the modifications of IRS1 may be a marker of early detection of Aβ42 elevation prior to the onset of memory decline in AD.

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