scholarly journals Clinical-phenomenological structure and age-related features of the course of the disease in adolescence with mild mental retardation

2021 ◽  
pp. 36-41
Author(s):  
Serhii Chabaniuk
Keyword(s):  
Mental Retardation ◽  
Family History ◽  
Term Treatment ◽  
Social Adaptation ◽  
Psychomotor Development ◽  
Mild Mental Retardation ◽  
Age Related ◽  
Long Term Treatment ◽  
Intellectual Deficit ◽  
Mental Pathology

Among the forms of mental pathology that are found in childhood, a special place is occupied by mental retardation, which makes a significant contribution to the rates of morbidity and disability. In order to establish the patterns of the clinical-phenomenological structure and age-specific course of the disease in adolescence with mild mental retardation, on the basis of the Kryvyi Rih neuropsychiatric dispensary, a two-stage clinical-epidemiological, clinical-psychopathological and psychodiagnostic study of 154 people born in 2003—2008 with mild mental disorders was carried out. According to the results of the study, it was found that the presence of mental retardation in most cases was diagnosed in the period of 7—10 years (29.8 % of cases), and in almost a third of all examined (29 %) this diagnosis was combined with concomitant psychiatric, neurological or somatic pathology, which just led to a deterioration in the general course of the disease. In 63 % cases there was a burdened family history, in 81 % — obstetric. In addition, a direct correlation (r = 0.498) was found between the level of development of social skills and the preservation of the intellectual level. Thus, it is possible to identify risk factors for the occurrence of mild mental retardation: male sex, family history (primarily addiction states), parents’ age over 30, their low educational level, pathological period of pregnancy and delayed psychomotor development in the first year of life. The level of social adaptation of patients depends on the depth of the intellectual deficit, long-term treatment and rehabilitation interventions, psycho-educational activities for parents and relatives, the organization of assistance in finding a job and medical support can increase the level of social adaptation of this contingent.

scholarly journals Suppression of AMD-Like Pathology by Mitochondria-Targeted Antioxidant SkQ1 Is Associated with a Decrease in the Accumulation of Amyloid β and in mTOR Activity

Antioxidants ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 177 ◽  
Author(s):  
Natalia A. Muraleva ◽  
Oyuna S. Kozhevnikova ◽  
Anzhela Z. Fursova ◽  
Nataliya G. Kolosova
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Developed Countries ◽  
Term Treatment ◽  
Age Related Macular Degeneration ◽  
Eye Health ◽  
Age Related ◽  
Long Term Treatment

Age-related macular degeneration (AMD) is a major cause of irreversible visual impairment and blindness in developed countries, and the molecular pathogenesis of AMD is poorly understood. Recent studies strongly indicate that amyloid β (Aβ) accumulation —found in the brain and a defining feature of Alzheimer’s disease—also forms in the retina in both Alzheimer’s disease and AMD. The reason why highly neurotoxic proteins of consistently aggregate in the aging retina, and to what extent they contribute to AMD, remains to be fully addressed. Nonetheless, the hypothesis that Aβ is a therapeutic target in AMD is debated. Here, we showed that long-term treatment with SkQ1 (250 nmol/[kg body weight] daily from the age of 1.5 to 22 months) suppressed the development of AMD-like pathology in senescence-accelerated OXYS rats by reducing the level of Aβ and suppressing the activity of mTOR in the retina. Inhibition of mTOR signaling activity, which plays key roles in aging and age-related diseases, can be considered a new mechanism of the prophylactic effect of SkQ1. It seems probable that dietary supplementation with mitochondria-targeted antioxidant SkQ1 can be a good prevention strategy to maintain eye health and possibly a treatment of AMD.

The Successful Long-Term Treatment of Age Related Erectile Dysfunction with hSlo cDNA in Rats In Vivo

2003 ◽  
Vol 170 (1) ◽  
pp. 285-290 ◽  
Author(s):  
A. MELMAN ◽  
W. ZHAO ◽  
K.P. DAVIES ◽  
R. BAKAL ◽  
G.J. CHRIST
Keyword(s):  
Erectile Dysfunction ◽  
Term Treatment ◽  
Age Related ◽  
Long Term Treatment

scholarly journals GDF11 induces differentiation and apoptosis and inhibits migration of C17.2 neural stem cells via modulating MAPK signaling pathway

2018 ◽  
Author(s):  
Zongkui Wang ◽  
Miaomiao Dou ◽  
Fengjuan Liu ◽  
Peng Jiang ◽  
Shengliang Ye ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Term Treatment ◽  
Population Doubling ◽  
Proteome Profiling ◽  
Positive Effects ◽  
Age Related ◽  
Long Term Treatment

GDF11, a member of TGF-β superfamily, has recently received widespread attention as a novel anti-ageing/rejuvenation factor to reverse age-related dysfunctions in heart and skeletal muscle, and to induce angiogenesis and neurogenesis. However, these positive effects of GDF11 were challenged by several other studies. Furthermore, the mechanism is still not well understood. In the present study, we evaluated the effects and underlying mechanisms of GDF11 on C17.2 neural stem cells. GDF11 induced differentiation and apoptosis, and suppressed migration of C17.2 neural stem cells. Besides, GDF11 slightly increased cell viability after 24h treatment, showed no effects on proliferation for about 10 days of cultivation, and slightly decreased cumulative population doubling for long-term treatment (p<0.05). Phospho-proteome profiling array displayed that GDF11 significantly increased the phosphorylation level of 13 serine/threonine kinases (p<0.01), including p-p38, p-ERK and p-Akt, in C17.2 cells, which implied the activation of MAPK pathway. Western blot validated that the results of phospho-proteome profiling array were reliable. Based on functional analysis, we demonstrated that the differentially expressed proteins were mainly involved in signal transduction which was implicated in cellular behavior. Collectively, our findings suggest that, for neurogenesis, GDF11 might not be the desired rejuvenation factor, but a potential target for pharmacologic blockade.

scholarly journals GDF11 induces differentiation and apoptosis and inhibits migration of C17.2 neural stem cells via modulating MAPK signaling pathway

2018 ◽  
Author(s):  
Zongkui Wang ◽  
Miaomiao Dou ◽  
Fengjuan Liu ◽  
Peng Jiang ◽  
Shengliang Ye ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Term Treatment ◽  
Population Doubling ◽  
Proteome Profiling ◽  
Positive Effects ◽  
Age Related ◽  
Long Term Treatment

GDF11, a member of TGF-β superfamily, has recently received widespread attention as a novel anti-ageing/rejuvenation factor to reverse age-related dysfunctions in heart and skeletal muscle, and to induce angiogenesis and neurogenesis. However, these positive effects of GDF11 were challenged by several other studies. Furthermore, the mechanism is still not well understood. In the present study, we evaluated the effects and underlying mechanisms of GDF11 on C17.2 neural stem cells. GDF11 induced differentiation and apoptosis, and suppressed migration of C17.2 neural stem cells. Besides, GDF11 slightly increased cell viability after 24h treatment, showed no effects on proliferation for about 10 days of cultivation, and slightly decreased cumulative population doubling for long-term treatment (p<0.05). Phospho-proteome profiling array displayed that GDF11 significantly increased the phosphorylation level of 13 serine/threonine kinases (p<0.01), including p-p38, p-ERK and p-Akt, in C17.2 cells, which implied the activation of MAPK pathway. Western blot validated that the results of phospho-proteome profiling array were reliable. Based on functional analysis, we demonstrated that the differentially expressed proteins were mainly involved in signal transduction which was implicated in cellular behavior. Collectively, our findings suggest that, for neurogenesis, GDF11 might not be the desired rejuvenation factor, but a potential target for pharmacologic blockade.

L-dopa long-term treatment in Parkinson's disease: Age-related side effects

Neurology ◽  
1983 ◽  
Vol 33 (11) ◽  
pp. 1518-1518 ◽  
Author(s):  
M. Pederzoli ◽  
F. Girotti ◽  
G. Scigliano ◽  
G. Aiello ◽  
F. Carella ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Term Treatment ◽  
Age Related ◽  
Long Term Treatment

scholarly journals Long-term treatment with aldosterone slows the progression of age-related hearing loss

2016 ◽  
Vol 336 ◽  
pp. 63-71 ◽  
Author(s):  
Joshua Halonen ◽  
Ashley S. Hinton ◽  
Robert D. Frisina ◽  
Bo Ding ◽  
Xiaoxia Zhu ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Term Treatment ◽  
Age Related ◽  
Long Term Treatment ◽  
Age Related Hearing Loss

scholarly journals Gleevec shifts APP processing from a β-cleavage to a nonamyloidogenic cleavage

2017 ◽  
Vol 114 (6) ◽  
pp. 1389-1394 ◽  
Author(s):  
William J. Netzer ◽  
Karima Bettayeb ◽  
Subhash C. Sinha ◽  
Marc Flajolet ◽  
Paul Greengard ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Amyloid Β ◽  
Term Treatment ◽  
App Processing ◽  
Age Related ◽  
Bace Inhibitor ◽  
Long Term Treatment ◽  
App Metabolism ◽  
High Concentrations ◽  
In Cells

Neurotoxic amyloid-β peptides (Aβ) are major drivers of Alzheimer’s disease (AD) and are formed by sequential cleavage of the amyloid precursor protein (APP) by β-secretase (BACE) and γ-secretase. Our previous study showed that the anticancer drug Gleevec lowers Aβ levels through indirect inhibition of γ-secretase activity. Here we report that Gleevec also achieves its Aβ-lowering effects through an additional cellular mechanism. It renders APP less susceptible to proteolysis by BACE without inhibiting BACE enzymatic activity or the processing of other BACE substrates. This effect closely mimics the phenotype of APP A673T, a recently discovered mutation that protects carriers against AD and age-related cognitive decline. In addition, Gleevec induces formation of a specific set of APP C-terminal fragments, also observed in cells expressing the APP protective mutation and in cells exposed to a conventional BACE inhibitor. These Gleevec phenotypes require an intracellular acidic pH and are independent of tyrosine kinase inhibition, given that a related compound lacking tyrosine kinase inhibitory activity, DV2-103, exerts similar effects on APP metabolism. In addition, DV2-103 accumulates at high concentrations in the rodent brain, where it rapidly lowers Aβ levels. This study suggests that long-term treatment with drugs that indirectly modulate BACE processing of APP but spare other BACE substrates and achieve therapeutic concentrations in the brain might be effective in preventing or delaying the onset of AD and could be safer than nonselective BACE inhibitor drugs.

Sign in / Sign up

Export Citation Format

Share Document