BACKGROUND:Researches on diagnosis and treatment of Alzheimer's disease, the most common type of dementia, are still ongoing. Taurine is frequently used in Alzheimer's disease models due to its protective effects. Metal cation dyshomeostasis is an important etiological factor for Alzheimer's disease. Transthyretin protein is thought to act as a transporter for the Aβ protein that accumulates in the brain and is eliminated in the liver and kidneys via the LRP-1 receptor. However, the effect of taurine on this mechanisms is not fully known. METHODS:30 male rats, aged 28 ± 4 months, were divided into 5 groups (n = 6) as follows: control group, sham group, Aβ 1-42 group, taurine group and taurine+Aβ 1-42 group. Oral taurine pre-supplementation was given as 1000 mg/kg-body weight/day for 6 weeks to taurine and taurine+Aβ 1-42 groups. RESULTS:Plasma copper, heart transthyretin and Aβ 1-42, brain and kidney LRP-1 levels were found to be decreased in the Aβ 1-42 group. Brain transthyretin was higher in taurine+Aβ 1-42 group and brain Aβ 1-42 was higher in Aβ 1-42 and taurine+Aβ 1-42 groups. CONCLUSION:Taurine pre-supplementation maintained cardiac transthyretin levels, decreased cardiac Aβ 1-42 levels and increased brain and kidney LRP-1 levels. Taurine may have a potential to be used as a protective agent for aged people at high risk for Alzheimer's disease.

Alzheimer's disease affects large populations worldwide. However, there is not yet a blood-based minimally invasive biomarker that can provide a definitive diagnosis. There is also no curative treatment. Extracellular senile amyloid plaques, which are formed by the accumulation of amyloid derivatives in the central nervous system, have an important role in the development of Alzheimer's disease. The reason for the accumulation of amyloid derivatives in the central nervous system is shown as excess production by faulty proteolysis of amyloid precursor protein by enzymes. However, one of the causes of amyloid deposition in the central nervous system is insufficient clearance of these derivatives. Since amyloid production cannot be balanced with amyloid clearance in Alzheimer's disease, accumulation of monomers, oligomers, insoluble fibrils and plaques is observed in the central nervous system. It is argued that the deficiency or loss of function of the transthyretin transporter protein, which is thought to be involved in this removal, and LRP-1, a blood-brain barrier receptor, also may predispose to Alzheimer's disease. In this review, possible biomarkers for Alzheimer's disease, transthyretin and LRP-1-mediated amyloid clearance were examined.

Objective. This systematic review was conducted to assess the sensitivity rate of SARS-CoV-2 detection in the saliva of ambulatory asymptomatic and mildly symptomatic patients, with saliva being collected passively without any forceful coughing. Study design: A literature search was performed from January 2020 to July 2021. Prospective studies excluding letters to editors were included in our review only if saliva and nasopharyngeal samples were collected simultaneously and sensitivity was reported using reverse transcription polymerase chain reaction (RT-PCR) in asymptomatic or mildly symptomatic ambulatory cases. Results: A total of 436 studies were assessed; 10 (4 cohorts and 6 cross-sectional) studies met our inclusion criteria. The sensitivity rate of saliva to detect SARS-CoV-2 varied from 85.7% to 98.6% in all except for 3 studies. Lower sensitivity levels were attributed to low viral load (51.9% and 63.8%) or lack of supervision while collecting saliva (66.7%). Conclusions. Passively collected saliva in the absence of coughing has a high sensitivity rate to detect SARS-CoV-2 in asymptomatic and mildly symptomatic patients compared with nasopharyngeal swabs. Limitations of previous studies, such as lack of attention to the method of saliva collection, stages, and severity of the disease at the time of sample collection, can be researched in future investigations.

The human bladder maintains a cycle of filling, storing, and micturating throughout an individual’s lifespan. The cycle relies on the ability of the bladder to expand without increasing the intravesical pressure, which is only possible with the controlled relaxation of well-complaint muscles and the congruously organized construction of the bladder wall. A competent bladder outlet, which functions in a synchronous fashion with the bladder, is also necessary for this cycle to be completed successfully without deterioration. In this paper, we aimed to review the contemporary physiological findings on bladder physiology and examine the effects of amino acids on clinical conditions affecting the bladder, with special emphasis on the available therapeutic evidence and possible future roles of the amino acids in the treatment of the bladder-related disorders.

Background/aim Physical exercise is a state of physiological stress that requires adaptation of the organism to physical activity. Glycogen is an important and essential energy source for muscle contraction. Skeletal muscle and liver are two important glycogen stores, and the energy required to maintain exercise in rodents are provided by destruction of this glycogen depot. In this study, the effects of endogenous opioid peptide antagonism at the central nervous system level on tissue glycogen content after exhaustive exercise were investigated. Materials and methods Rats had intracerebroventricularly (icv) received nonspecific opioid peptide receptor antagonist, naloxone (50 μg/10 μL in saline) and δ-opioid receptor-selective antagonist naltrindole (50 μg/10 μL in saline) and then exercised till exhaustion. After exhaustion, skeletal muscle, heart, and liver were excised immediately. Results Both opioid peptide antagonists decreased glycogen levels in skeletal muscle. Although, in soleus muscle, this decrease was not statistically significant (p > 0.05), in gastrocnemius muscle, it was significant in the icv naloxone administered group compared with control (p < 0.05). Heart glycogen levels increased significantly in both naloxone and naltrindole groups compared to control and sham-operated groups (p < 0.05). Heart glycogen levels were higher in the naloxone group than naltrindole (p < 0.05). Liver glycogen levels were elevated significantly with icv naloxone administration compared with the control group (p < 0.05). Glycogen levels in the naloxone group was also significantly higher than the naltrindole group (p < 0.05). Conclusion Our findings indicate that icv administered opioid peptide antagonists may play a role in glycogen metabolism in peripheral tissues such as skeletal muscle, heart, and liver.

Objective: The aim of our study is to investigate the change of peroxisomal proteins in the neurodegenerative and oxidative process caused by the neurotoxicity of A beta 1-42 in aged rats supplemented with taurine and to show the possible positive effects of taurine in this process. Methods: 30 Wistar albino rats were randomly divided into 5 groups as control, sham, A beta 1-42, taurine, and A beta 1-42+taurine. Taurine administration continued for 6 weeks (1000 mg/kg/day with drinking water). Stereotaxic surgery was applied to all groups (intracerebroventricular per lateral ventricle needle only or 5 mu l, PBS, or A beta 1-42). Spatial learning and memory performances of the animals were evaluated with Morris water maze and elevated plus maze. The levels of MDA and GSH were measured as oxidative stress parameters in the cerebral cortex and hippocampus. Expressions of CAT, PEX14, PMP70 of peroxisomal membrane proteins were indicated by Western blot analysis. Results: Our results showed that injection of A beta 1-42 decreased the spatial learning and memory performance, cortex CAT and hippocampus PEX14, PMP70 and GSH levels, and increased cortex and hippocampus MDA levels (p < 0.05). Although the administration of taurine partially ameliorated the adverse effects of A beta 1-42 injection, a significant difference was found only at the hippocampus GSH levels (p < 0.05). Also, taurine caused anxiety at this dose (p < 0.05). Discussion: In conclusion, decreased peroxisomal proteins and antioxidant capacity in neurodegenerative and oxidative processes induced by intracerebroventricular A beta 1-42 injection showed that peroxisomes may play a role in this process and taurine supplementation may have positive effects especially in increasing antioxidant capacity.

Taurine, 2-aminoethanesulfonic acid is an important endogenous amino acid found in the central nervous system. In our body, it plays a role in many physiological mechanisms such as central nervous system development, thermoregulation, anti-inflammatory effects, antioxidation, osmoregulation, calcium homeostasis. Due to these beneficial effects, taurine has become popular recently. Taurine is found in many products we use in our daily life. However, according to recent research, it was not found to be completely safe. It is very important to examine the use of taurine due to increased use. Therefore, based on our studies and other studies in the literature; we tried to examine the beneficial and harmful effects of taurine, the appropriate dose amount and its role in the neurodegenerative process in this review.

Background/aim The purpose of the present study was to explore the neuroprotective role of delta opioid receptors (DOR) in the rat cortex in hypoxic preconditioning. Materials and methods Rats were randomly divided into 8 groups: control (C), sham (S), hypoxic preconditioning (PC), severe hypoxia (SH), PC + SH, PC + SH + Saline (PS), PC + SH + DPDPE (DPDPE, selective DOR agonist), PC + SH + NT (NT, Naltrindole, selective DOR antagonist). Drugs were administered intracerebroventrically. Twenty four h after the end of 3 consecutive days of PC (10% O2, 2 h/day), the rats were subjected to severe hypoxia (7% O2 for 3 h). Bcl-2 and cyt-c were measured by western blot, and caspase-3 was observed immunohistochemically. Results Bcl-2 expressions in the PC group were higher than in control, SH, and PC + SH groups. Even though there were no significant differences between the groups in terms of cyt-c levels, caspase-3 immunoreactivity of cortical neurons and glial cells in the severe hypoxia and NT groups were higher than in the control, sham, and hypoxic preconditioning groups. DPDPE administration diminished caspase-3 immunoreactivity compared with all of the severe hypoxia groups. Conclusions These results suggest that cortical cells are resistant to apoptosis via increased expression of Bcl-2 and decreased immunoreactivity of caspase-3 in the cortex, and that DOR is involved in neuroprotection induced by hypoxic preconditioning via the caspase-3 pathway in cortical neurons.