جستجوی مقالات مرتبط با کلیدواژه « Amyloid » در نشریات گروه « پزشکی »

Neurodegenerative diseases (NDDs) cause progressive neuronal loss, resulting in morbidity and mortality. Research is continued on treatment strategies that can tackle the disease's pathophysiology and cease its progression. Considering the anti-apoptotic and neuroprotective properties of apelin, we hypothesized that apelin-13 could be a therapeutic solution for Alzheimer's disease and similar NDDs. Therefore, we evaluated its effect on scopolamine-treated rats.

Male rats (n=40) were assigned to 5 groups of 8. No intervention was considered for the control group. The scopolamine group received stereotaxic surgery and was treated with 3 mg/kg scopolamine intraperitoneally. The treatment groups were treated with scopolamine plus intraventricular injection of apelin-13 (1.25, 2.5, and 5 µg) into the right lateral ventricles for 7 days. For evaluating the memory impairment, the passive avoidance reactions of the animals, except the control group, were assessed 24 hours following the last injection. Regarding histological analysis, Congo red staining of the hippocampal sections was done, and immunoblotting was used to determine apoptotic biochemical markers, including caspase 3, cytochrome C, and congophilic amyloid-beta plaques.

Apelin–13 alleviated scopolamine-related passive avoidance memory impairment and reduced the number of congophilic amyloid-beta plaques in the hippocampus (all P<0.001). It attenuated the decrease in the mean levels of hippocampal apoptotic proteins (caspase 3, cytochrome C) in animals treated with scopolamine (all P<0.05).

The neuroprotective effects of apelin-13 suggest its therapeutic effect on neurodegenerative disorders.

We evaluated the relationship between regional accumulations of the tau positron emission tomography (PET) tracer THK5351 and cognitive dysfunction in the Alzheimer's disease (AD) continuum.

The cases of 18 patients with AD or mild cognitive impairment (MCI) due to AD who underwent three-dimensional MRI, fluoro-2-deoxyglucose (FDG)-(PET), Pittsburgh compound B (PiB)-amyloid PET, and THK5351-tau PET were analyzed. Their mean age was 70.6±11.3, their mean Mini-Mental State Examination (MMSE) score was 22.3±6.8, and their mean Alzheimer Disease Assessment Scale-Cognitive Subtest (ADAS) score was 12.5±7.3. To determine the correlation between each patient's four imaging results and their MMSE and ADAS scores, we performed a voxel-wise statistical analysis with statistical parametric mapping (SPM).

The SPM analysis showed that the bilateral parietotemporal FDG accumulations and MMSE scores were positively correlated, and the bilateral parietotemporal FDG accumulations were negatively correlated with ADAS scores. There were significant correlations between bilateral parietotemporal and left posterior cingulate/precuneus THK5351 accumulations and MMSE/ADAS scores.

In the AD brain, THK5351 correlates with neuropsychological test scores as well as or more additional than FDG due to its affinity for both tau and monoamine oxidase-B (MAO-B), and measurements of THK5351 may thus be useful in estimating the progression of AD.

A variety of cytokines are involved in cognitive functioning. Balance restoration between protective and degenerative neuro-inflammation is of great interest in newer therapeutic approaches. In the current study, we investigated the effect of pramipexole (PMX) on memory functions, hippocampal amyloid deposition, serum cytokines, and brain-derived neurotrophic factor (BDNF)  levels in lipopolysaccharide (LPS) challenged-rats.

Male Wistar rats were divided into 5 groups (n=8): control (saline), lipoppolysacharide (LPS 250 mcg/kg bw), and experimental groups (LPS and PMX 0.5, 1, and 3 mg/kg bw). Learning and memory were assessed by the novel object recognition test (NORT), Y-maze, and step-through test. Immunological and histological assays were performed.

In memory tasks, LPS-challenged rats showed reduction in the observed parameters. In NORT, PMX 1 mg/kg increased recognition index compared with controls, whereas the other two doses increased this index only against the LPS-control. In Y-maze, all doses of PMX significantly had increased alternation when compared with LPS. In the step-through test, only the lowest dose of PMX extended the latency compared with LPS. Histological examination revealed that PMX at doses of 0.5 and 1 mg/kg reduced amyloid deposition in the hippocampus. Interleukin (IL)-10 serum levels were elevated by 1 mg/kg PMX. Tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 serum levels remained under the detectable minimum in all experimental groups. PMX at all doses significantly decreased BDNF serum concentration.

In rats with LPS-induced neuro-inflammation PMX improved hippocampal-dependent memory and exerted immuno-modulatory effects by increasing IL-10.

Alzheimer disease (AD) is characterized by the decline of cognitive functions such as learning and memory. Scientific society has proposed some non-pharmacological interventions, among which photobiomodulation has gained prominence for its beneficial effects. Therefore, we investigated, through systematic review, the therapeutic potential of photobiomodulation in AD.

This systematic review was registered under the number CRD42019128416 in the International Prospective Record of Systematic Reviews (PROSPERO). A systematic search was conducted on the bibliographic databases (PubMed and ScienceDirect) with the keywords based on MeSH terms: “photobiomodulation therapy” or “low-level laser therapy” or “LLLT” or “light emitting diode” and “amyloid” or “Alzheimer”. The data search was conducted from 2008 to 2019. We follow the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline. The search strategy included experimental in vivo and in vitro studies in the English language and photobiomodulation as a non-pharmacological intervention. We included 10 studies, being 5 in vivo studies, 4 in vitro studies and 1 study using in vivo and in vitro. To evaluate the quality of the studies, we used the Rob tool of the Systematic Review Center for Laboratory Animal Experimentation (SYRLE).

The studies showed that photobiomodulation is able to reduce inflammatory response, oxidative stress and apoptotic effects generated by amyloid beta (Aβ) and restore mitochondrial function and cognitive behavior.

Taken together, these results indicate that photobiomodulation may be a useful tool for treating AD

Formation of amyloid fibrils has been associated with different protein aggregation diseases. Many studies indicate that many proteins can be converted in vitro into amyloid structures. Isolated ҡ-casein (ҡ-CN) spontaneously forms amyloid fibrils under physiological conditions, so it is a convenient model for researching generic aspect of fibril formation. The aim of this study was to test in vitro the ability of S. rosmarinus extract to inhibit the formation of amyloid fibrils in ҡ-CN.

In this study the effect of aqueous extract of S. rosmarinus on the amyloid formation of ҡ-CN in the presence and absence of crowding agent, dextran, have been examined using Thioflavin T binding (ThT) assay, fluorescence spectroscopy, and circular dichroism (CD) spectroscopy.

ThT binding assay showed that dextran increased the rate of amyloid fibril formation and S. rosmarinus extract retarded the amyloid fibril formation in κ-CN. In the presence of dextran however, the effect of S. rosmarinus extract on the amyloid formation of ҡ-CN was less than in its absence. Fluorescence spectroscopy results also demonstrated that dextran led to unfolding and increased the exposure hydrophobic area in ҡ-CN. S. rosmarinus extract efficiency decreased the exposure of hydrophobic regions in κCN, whereas in the presence of dextran this effect of extract was reduced. CD spectroscopy results exhibited that incubation of κ-CN with S. rosmarinus extract prevented a structural transition to a β-sheet. CD spectroscopy results also indicated that by adding dextran to reduced κ-CN β-sheet structures observed, which indicates structural change. S. rosmarinus extract however, prevented transition to β-sheet structural.

In conclusion our finding suggests that S. rosmarinus extract prevents amyloid fibril formation in κ-CN, although this effect decreased in the presence of dextran.