Brain Tissue Extracts Research Articles

Current safety recommendations for handling mouse and human αsynuclein pre-formed fibrils.

α-Synuclein (α-syn) can form amyloid fibrils. Lewy bodies and Lewy neurites containing aggregated α-syn are pathological markers of Parkinson's Disease and Dementia with Lewy Bodies. To better understand the role of pathological α-syn in disease, many labs use α-syn preformed fibrils (PFFs). Neurons take up the PFFs, which act as seeds to corrupt endogenously expressed α-syn, inducing it to form aggregates very similar to those found in diseased brains. The PFFs are typically generated using recombinant mouse or human α-syn. α-Syn fibrils can also be extracted or amplified from brain tissue extracts, cerebrospinal fluid, or skin biopsies from patients with known synucleinopathy. The PFFs are then added to cell culture, or injected into rodents or primates to induce pathology. Because PFFs can corrupt endogenous α-syn, researchers should adhere to strict safety protocols when handling PFFs to minimize potential exposures. Our group consulted with biosafety professionals at the University of Alabama at Birmingham (UAB) to identify potential risks related to working with α-syn PFFs and offer containment controls to mitigate those risks. Potential exposures include pipetting, opening tubes, and sonication of the PFFs to generate fragments, all of which could potentially generate aerosols. Here, we outline best practices for the safe conduct of research with α-syn fibrils, including personal protective equipment and decontamination procedures. We highlight steps in which extra precautions should be taken and how to minimize exposure and potential risk associated with use of PFFs in scientific research.

Isolation of Amyloid Fibrils from Brain Tissue Extract

Isolation of Amyloid Fibrils from Brain Tissue Extract

Isolation of Amyloid Fibrils from Brain Tissue Extract

Isolation of Amyloid Fibrils from Brain Tissue Extract

Diffusion Basis Spectrum Imaging in Midlife Obesity: Associations with Abdominal Adipose Tissue

AbstractBackgroundObesity and abdominal adiposity in midlife are shown to increase the risk of Alzheimer disease. However, it is not clear whether midlife adiposity is associated with increased neuroinflammation. We aimed to investigate the associations of obesity, BMI of 30 kg/m2 or higher, and abdominal visceral and subcutaneous adipose tissue (VAT and SAT) with brain histology, using diffusion basis spectrum imaging (DBSI) analysis;MethodIn total, 54 cognitively normal middle‐aged subjects (50.46±6.19 years, male: 21 (38.9%), obesity: 32 (59.3 %), BMI: 32.18±6.99 kg/m2) underwent brain and abdominal 3T MRI. Abdominal VAT and SAT were semi‐automatically segmented using VOXel Analysis Suite (Voxa). A DBSI scheme with a total of 98 diffusion samplings was acquired followed by movement and eddy current correction and brain tissue extraction in FSL. DBSI maps including fractional anisotropy (FA, overall integrity), axial diffusivity (AD, axonal injury), radial diffusivity (RD, myelin loss), restricted fraction (RF, inflammation cellularity), hindered fraction (HF, extracellular edema), and fiber fraction (FF, axonal density) were generated using in‐house software scripted in MATLAB. DBSI‐derived maps were processed using a tract‐based spatial statistics (TBSS) pipeline for whole‐brain white matter voxel‐wise analyses. Using the Randomize tool from FSL, the difference between obese vs. non‐obese, high‐VAT vs. low‐VAT, and high‐SAT vs. low‐SAT groups were investigated for each DBSI‐derived skeleton, with age and sex as covariates, and a threshold of 0.05 for false‐discovery rate. The sex differences were further investigated;ResultLower FF and AD and higher RF in widespread white matter areas were observed in the obese vs. non‐obese group, and in the high‐SAT vs. low‐SAT group. Lower AD and higher RF were observed for the high‐VAT vs. low‐VAT group. All of these differences were only significant in females, not males, but higher RF in obese vs. non‐obese was observed both in males and females;ConclusionOur data support lower axonal density and fiber integrity, as well as higher inflammation cellularity in cognitively normal, middle‐aged obese individuals, and those with high VAT and high SAT, especially in females. Overall, our data suggest the differential role of visceral and subcutaneous abdominal fat in promoting neuroinflammation and axonal damage.

Extraction of In-Cell β-Amyloid Fibrillar Aggregates for Studying Molecular-Level Structural Propagations Using Solid-State NMR Spectroscopy.

Molecular-level structural polymorphisms of β-amyloid (Aβ) fibrils have recently been recognized as pathologically significant. High-resolution solid-state nuclear magnetic resonance (ssNMR) spectroscopy has been utilized to study these structural polymorphisms, particularly in ex-vivo fibrils seeded from amyloid extracts of post-mortem brain tissues of Alzheimer's disease (AD) patients. One unaddressed question in current ex-vivo seeding protocol is whether fibrillation from exogenous monomeric Aβ peptides, added to the extracted seeds, can be quantitatively suppressed. Addressing this issue is critical because uncontrolled fibrillation could introduce biased molecular structural polymorphisms in the resulting fibrils. Here, we present a workflow to optimize the key parameters of ex-vivo seeding protocols, focusing on the quantification of amyloid extraction and the selection of exogenous monomeric Aβ concentrations to minimize nonseeded fibrillation. We validate this workflow using three structurally different 40-residue Aβ (Aβ40) fibrillar seeds, demonstrating their ability to propagate their structural features to exogenous wild-type Aβ40.

Fructose-2,6-bisphosphate restores DNA repair activity of PNKP and ameliorates neurodegenerative symptoms in Huntington’s disease

Huntington's disease (HD) and spinocerebellar ataxia type 3 (SCA3) are the two most prevalent polyglutamine (polyQ) neurodegenerative diseases, caused by CAG (encoding glutamine) repeat expansion in the coding region of the huntingtin (HTT) and ataxin-3 (ATXN3) proteins, respectively. We have earlier reported that the activity, but not the protein level, of an essential DNA repair enzyme, polynucleotide kinase 3'-phosphatase (PNKP), is severely abrogated in both HD and SCA3 resulting in accumulation of double-strand breaks in patients' brain genome. While investigating the mechanistic basis for the loss of PNKP activity and accumulation of DNA double-strand breaks leading to neuronal death, we observed that PNKP interacts with the nuclear isoform of 6-phosphofructo-2-kinase fructose-2,6-bisphosphatase 3 (PFKFB3). Depletion of PFKFB3 markedly abrogates PNKP activity without changing its protein level. Notably, the levels of both PFKFB3 and its product fructose-2,6 bisphosphate (F2,6BP), an allosteric modulator of glycolysis, are significantly lower in the nuclear extracts of postmortem brain tissues of HD and SCA3 patients. Supplementation of F2,6BP restored PNKP activity in the nuclear extracts of patients' brain. Moreover, intracellular delivery of F2,6BP restored both the activity of PNKP and the integrity of transcribed genome in neuronal cells derived from the striatum of the HD mouse. Importantly, supplementing F2,6BP rescued the HD phenotype in Drosophila, suggesting F2,6BP to serve in vivo as a cofactor for the proper functionality of PNKP and thereby, of brain health. Our results thus provide a compelling rationale for exploring the therapeutic use of F2,6BP and structurally related compounds for treating polyQ diseases.

Subject-Specific Probability Maps of Scalp, Skull and Cerebrospinal Fluid for Cranial Bones Segmentation in Neonatal Cerebral MRIs

ObjectivesSegmentation of cranial bones in magnetic resonance images (MRIs) is a challenging and indispensable task to study neonatal brain development and injury. This paper presents a new approach for creating subject-specific probability maps of the scalp, skull and cerebrospinal fluid (CSF) from retrospective bimodal (MR and CT) images acquired from neonates in the gestational age range of 39 to 42 weeks. These maps are subsequently employed for the segmentation of cranial bones in cerebral MRIs from neonates in the same age range. Material and methodsRetrospective MR and CT of neonates with normal head in the gestational age range of 39-42 weeks were preprocessed, segmented semi-automatically and employed as atlas data. For an input MR image acquired from a subject under study, a preprocessing stage and three main processing blocks were performed: First, subject-specific head and intracranial templates and CSF probability map were created using retrospective MR atlas data. Second, the CT atlas data were coregistered to MR templates and the resulted deformation matrices were fed to the next block to create subject-specific scalp and skull probability maps. Finally, some novel performance measures were presented to evaluate the performance of subject-specific CSF, scalp and skull probability maps for skull and intracranial segmentation in neonatal MRIs. ResultsThe subject-specific probability maps were employed for brain tissue extraction and compared with two public methods such as Brain Extraction Tool (BET) and Brain Surface Extractor (BSE). They were also applied for cranial bone extraction. Then, the similarity in shape between the frontal and occipital sutures (which had been reconstructed from segmented cranial bones) and the ground truth landmarks was evaluated. For this purpose, modified versions of the Dice similarity coefficient (DSC) were used. Finally, a retrospective bimodal (MR-CT) data acquired from a neonate within a short time interval was used for evaluation. After co-alignment of the two images, the DSC and modified Hausdorff distance (MHD) were used to compare the similarity of cranial bones in the MR and CT images. ConclusionSignificant improvements were achieved compared to conventional methods which rely solely on MR image intensities. These advancements hold promise for enhancing neurodevelopmental studies in neonates. The algorithm for creating subject-specific atlases is publicly accessible through a graphical user interface at medvispy.ee.kntu.ac.ir.

A comprehensive assessment of the cholinergic-supporting and cognitive-enhancing effects of Rosa damascena Mill. (Damask rose) essential oil on scopolamine-induced amnestic rats.

Alzheimer's disease (AD) is a neurodegenerative condition characterized by gradual loss of cognitive abilities (dementia) and is a major public health problem. Here, we aimed at investigating the effects of Rosa damascena essential oil (RDEO) on learning and memory functions in a rat model of amnesia induced by scopolamine, as well as on changes in acetylcholinesterase (AChE) activity, M1 muscarinic acetylcholine receptor (mAChR) expression, and brain-derived neurotrophic factor (BDNF) levels in the extracted brain tissues. The control, amnesia (scopolamine, 1mg/kg/i.p.) and treatment (RDEO, 100μL/kg/p.o. or galantamine, 1.5mg/kg/i.p.) groups were subjected to Morris water maze and new object recognition tests. AChE activity was assayed by ELISA, and M1 mAChR and BDNF concentration changes were determined by western blotting. Also, using computational tools, human M1 mAChR was modeled in an active conformation, and the major components of RDEO were docked onto this receptor. According to our behavioral tests, RDEO was able to mitigate the learning and memory impairments caused by scopolamine in vivo. Our in vitro assays showed that the observed positive effects correlated well with a decrease in AChE activity and an increase in M1 mAChR and BDNF levels in amnestic rat brains. We also demonstrated in an in silico setting that the major components of RDEO, specifically -citronellol, geraniol, and nerol, could be accommodated favorably within the allosteric binding pocket of active-state human M1 mAChR and anchored here chiefly by hydrogen-bonding and alkyl-π interactions. Our findings offer a solid experimental foundation for future RDEO-based medicinal product development for patients suffering from AD.

Enrichment and MALDI-TOF MS Analysis of Phosphoinositides in Brain Tissue.

Triazolium cyclodextrin click cluster (+CCC) is an ideal scaffold to specifically bind phosphoinositides (PIPs) via multivalent electrostatic interaction. A new enrichment material, triazolium cyclodextrin click cluster-magnetic agarose bead conjugate (+CCC-MAB), was synthesized and applied to the PIP enrichment of brain tissue. The enriched sample was analyzed using MALDI-TOF MS in negative ion mode without any derivatization. The PIP extract of brain tissue is known to contain abundant lipid interferences. By employing magnetic pull-down separation using +CCC-MAB, we effectively removed the weak-binding interferences in the PIP extract, thereby improving the signal-to-noise ratio (S/N) of the PIPs. Our +CCC-MAB-based PIP enrichment enabled us to analyze 16 PIP species in brain tissue. Six species with high S/N were assigned by MS/MS, while the remaining 10 species with low S/N were characterized by an empirical selection guide based on the biological relevance of PIPs. We conclude that +CCC-MAB-based PIP enrichment is a promising MALDI sample preparation method for specific PIP analysis in brain tissue.

Melatonin's Protective Effects on Neurons in an in Vitro Cell Injury Model.

Currently, the role of melatonin (MT) in neuronal damage remains unclear and this study aimed to explore the protective effects of MT on neurons in an in vitro cell injury model. The Sprague Dawley (SD) rat traumatic brain injury (TBI) model was prepared, and brain tissue extract (BTE) from the injured area were generated. To establish a cell injury model in vitro, the BTE was added to the culture medium during the neuron culture process. MT was introduced into the culture medium of the cell injury model to observe its protective effects on neurons. Relevant molecular biology experiments were conducted to observe cellular oxidative stress status, inflammation, endoplasmic reticulum (ER) stress, mitochondrial damage, and neuronal apoptosis. When compared to the control group, the BTE group exhibited a significant increase in cellular oxidative stress, inflammation, neurofilament light polypeptide (NEFL) expression, and ER stress. Additionally, the mitochondrial DNA (mtDNA) copy number significantly decreased, and there was a higher count of apoptotic cells (p < 0.05). Upon the addition of MT to the culture medium of the in vitro cell injury model, there was a significant reduction in cellular oxidative stress, inflammation, and NEFL levels. This addition also mitigated ER stress, increased mtDNA copy numbers, and decreased the ratio of cell apoptosis (p < 0.05). In the in vitro cell injury model, MT demonstrates the capacity to inhibit cellular oxidative stress, inflammation, and ER stress levels. Additionally, it diminishes mtDNA damage, fosters cell viability, and serves as a protective agent against both apoptosis and necrosis in neurons.

Effects of Social Defeat Stress on Microtubule Regulating Proteins and Tubulin Polymerization.

: Microtubule (MT) stability in neurons is vital for brain development; instability is associated with neuropsychiatric disorders. The present study examined the effects of social defeat stress (SDS) on MT-regulating proteins and tubulin polymerization. : After 10 days of SDS, defeated mice were separated into susceptible (Sus) and unsusceptible (Uns) groups based on their performance in a social avoidance test. Using extracted brain tissues, we measured the expression levels of α-tubulin, acetylated α-tubulin, tyrosinated α-tubulin, MT-associated protein-2 (MAP2), stathmin (STMN1), phospho stathmin serine 16 (p-STMN1 [Ser16]), phospho stathmin serine 25 (p-STMN1 [Ser25]), phospho stathmin serine 38 (p-STMN1 [Ser38]), stathmin2 (STMN2), phospho stathmin 2 serine 73 (p-STMN2 [Ser73]), 78-kDa glucose-regulated protein (GRP-78), and CCAAT/enhancer binding protein (C/EBP)-homologous protein (CHOP) using Western blot assay. The tubulin polymerization rate was also measured. : We observed increased and decreased expression of acetylated and tyrosinated α-tubulin, respectively, decreased expression of p-STMN1 (Ser16) and increased expression of p-STMN1 (Ser25), p-STMN2 (Ser73) and GRP-78 and CHOP in the prefrontal cortex and/or hippocampus of defeated mice. A reduced tubulin polymerization rate was observed in the Sus group compared to the Uns and Con groups. : Our findings suggest that SDS has detrimental effects on MT stability, and a lower tubulin polymerization rate could be a molecular marker for susceptibility to SDS.

The Activity of Substance P (SP) on the Corneal Epithelium

In 1931, Von Euler and Gaddum isolated substance P (SP), an undecapeptide from the tachykinin family, from equine brain and intestine tissue extracts. Numerous types of cells, including neurons, astrocytes, microglia, epithelial, and endothelial cells, as well as immune cells including T-cells, dendritic cells, and eosinophils, are responsible for its production. The corneal epithelium, immune cells, keratocytes, and neurons all express the two isoforms of NK1R, which has the highest affinity for SP. The most recent research supports SP’s contribution to corneal healing by encouraging epithelial cell migration and proliferation. Additionally, when applied to the eyes, SP has proinflammatory effects that result in miosis, intraocular inflammation, and conjunctival hyperemia. In this review article, we examine the role of substance P within the eye. We focus on the role of SP with regards to maintenance and healing of the corneal epithelium.

Zinc deficiency and therapeutic role of sesame seeds on some physiological aspects of reproduction and growth in pregnant rats and its neonates

The present study aimed to find the Effect of zinc deficiency on some reproductive parameters among female rats and the growth of its neonates and to assess the therapeutic role of the sesame seeds. The research contained 35 pregnant females rats they were divided into seven groups, the first was control, the second was fed diet poor in zinc, the third group added sesame to diet poor in zinc and the fourth group was treated with diet poor in zinc added to it vitamin C. Groups five, six and seven were given poor zinc diet in the first, second and third trimester, respectively. The results showed a significant decrease of Prolactin (PRL) level in studied groups except in vitamin C group which showed no significant differences in value (P≤0.05) compared with a poor zinc diet group. While there were increasing in the FSH and LH levels in all studied groups except the first week which showed no significant difference compared with a poor zinc diet. Results indicated a significant decrease in the level of Estrogen(E2) in the first and third weeks, and increased its level in vitamin C and the second week groups, while sesame seeds group showed no significant difference compared with the poor zinc diet Group. The results showed an increased level of Progesterone (PRO) significantly in the second and the third week groups and a decrease in the sesame seeds and the first week groups, and the lack of significant difference in the vitamin C group compared with the poor zinc Group. The results showed a high level of superoxide dismutase( SOD) Glutathione (GSH) and low level of malondialdehyde (MDA) significantly in the studied groups except for the second week group appeared no significant difference in the level of GSH and MDA compared with a poor zinc diet group. The results of neonates showed significant increasing in the length of the body in sesame seeds and vitamin C groups, while showed no significant differences in the group of first, second and third weeks compared to poor zinc diet. Studied groups showed also a significant increase in body weight except for the second week group which showed a significant decrease, while the third week group did not show significant differences compared with the poor zinc diet Group. The results showed a significant decrease in mortality rate and the level of MDA in the brain, liver and placenta tissue extract in all groups except the second week group which showed a significant increase in the mortality rate and the level of liver MDA and placenta and in the first week in liver MDA only in comparison with a poor zinc diet group.

Automated tumor segmentation and brain tissue extraction from multiparametric MRI of pediatric brain tumors: A multi-institutional study.

Brain tumors are the most common solid tumors and the leading cause of cancer-related death among all childhood cancers. Tumor segmentation is essential in surgical and treatment planning, and response assessment and monitoring. However, manual segmentation is time-consuming and has high interoperator variability. We present a multi-institutional deep learning-based method for automated brain extraction and segmentation of pediatric brain tumors based on multi-parametric MRI scans. Multi-parametric scans (T1w, T1w-CE, T2, and T2-FLAIR) of 244 pediatric patients ( n = 215 internal and n = 29 external cohorts) with de novo brain tumors, including a variety of tumor subtypes, were preprocessed and manually segmented to identify the brain tissue and tumor subregions into four tumor subregions, i.e., enhancing tumor (ET), non-enhancing tumor (NET), cystic components (CC), and peritumoral edema (ED). The internal cohort was split into training ( n = 151), validation ( n = 43), and withheld internal test ( n = 21) subsets. DeepMedic, a three-dimensional convolutional neural network, was trained and the model parameters were tuned. Finally, the network was evaluated on the withheld internal and external test cohorts. Dice similarity score (median ± SD) was 0.91 ± 0.10/0.88 ± 0.16 for the whole tumor, 0.73 ± 0.27/0.84 ± 0.29 for ET, 0.79 ± 19/0.74 ± 0.27 for union of all non-enhancing components (i.e., NET, CC, ED), and 0.98 ± 0.02 for brain tissue in both internal/external test sets. Our proposed automated brain extraction and tumor subregion segmentation models demonstrated accurate performance on segmentation of the brain tissue and whole tumor regions in pediatric brain tumors and can facilitate detection of abnormal regions for further clinical measurements.

Tumoral and normal brain tissue extraction protocol for wide-scope screening of organic pollutants

Little is known about the presence of organic pollutants in human brain (and even less in brain tumors). In this regard, it is necessary to develop new analytical protocols capable of identifying a wide range of exogenous chemicals in this type of samples (by combining target, suspect and non-target strategies). These methodologies should be robust and simple. This is particularly challenging for solid samples, as reliable extraction and clean-up techniques should be combined to obtain an optimal result. Hence, the present study focuses on the development of an analytical methodology that allows the screening of a wide range of organic chemicals in brain and brain tumor samples. This protocol was based on a solid-liquid extraction based on bead beating, solid-phase extraction clean-up with multi-layer mixed-mode cartridges, reconstitution and LCHRMS analysis. To evaluate the performance of the extraction methodology, a set of 66 chemicals (e.g., pharmaceuticals, biocides, or plasticizers, among others) with a wide range of physicochemical properties was employed. Quality control parameters (i.e., linear range, sensitivity, matrix effect (ME%), and recoveries (R%)) were calculated and satisfactory results were obtained for them (e.g., R% within 60–120% for 32 chemicals, or ME% higher than 50% (signal suppression) for 79% of the chemicals).

A generalizable brain extraction net (BEN) for multimodal MRI data from rodents, nonhuman primates, and humans.

Accurate brain tissue extraction on magnetic resonance imaging (MRI) data is crucial for analyzing brain structure and function. While several conventional tools have been optimized to handle human brain data, there have been no generalizable methods to extract brain tissues for multimodal MRI data from rodents, nonhuman primates, and humans. Therefore, developing a flexible and generalizable method for extracting whole brain tissue across species would allow researchers to analyze and compare experiment results more efficiently. Here, we propose a domain-adaptive and semi-supervised deep neural network, named the Brain Extraction Net (BEN), to extract brain tissues across species, MRI modalities, and MR scanners. We have evaluated BEN on 18 independent datasets, including 783 rodent MRI scans, 246 nonhuman primate MRI scans, and 4601 human MRI scans, covering five species, four modalities, and six MR scanners with various magnetic field strengths. Compared to conventional toolboxes, the superiority of BEN is illustrated by its robustness, accuracy, and generalizability. Our proposed method not only provides a generalized solution for extracting brain tissue across species but also significantly improves the accuracy of atlas registration, thereby benefiting the downstream processing tasks. As a novel fully automated deep-learning method, BEN is designed as an open-source software to enable high-throughput processing of neuroimaging data across species in preclinical and clinical applications.

HPTLC method for effective separation of L-glutamic acid and GABA present in brain tissue extracts

L-glutamic acid and ϒ-aminobutyric acid (GABA) show similar physicochemical properties, so separating them by thin-layer chromatography (TLC) is difficult. TLC is currently a widely used method because of its simplicity, flexibility, and low cost compared to liquid or gas chromatography. This paper shows the TLC separation of [3H]glutamic acid from [3H]GABA formed by incubating the former with the membrane or the cytosolic fraction obtained from the locus coeruleous on the brain. Such separation was achieved with a better resolution than the literature reported. Radiolabeled compounds were extracted from the tissue and seeded on an HPTLC plate. In addition, placed the L-glutamic acid and GABA standards in different lanes. The plates were developed in a solvent system of butan-1-ol, acetic acid, and water = 5:3:2 (v:v), containing 0.4% ninhydrin as a derivatizing agent. HPTLC was used to obtain better resolving power, faster development times, less sample diffusion, and lower solvent consumption than TLC. Results showed that the L-glutamic acid and GABA standards were adequately separated, with a resolution of 2.2. Moreover, the studied tissue transformed 9% of the radiolabeled glutamate into GABA. The L-glutamic acid was converted into a fluorescent tautomer from Schiff's base, detectable on a λ=302 nm. However, when the HPTLC dried, the tautomer was identified as GABA for its Rf=0.32, and the luminescence disappeared. The resolution between both components was excellent (Rs=2.2). In conclusion, it was possible to develop a reproducible method from the data of this study, which could attract the interest of researchers.

Modeling the early stages of Alzheimer’s disease by administering intracerebroventricular injections of human native Aβ oligomers to rats

Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disease characterized by the accumulation of aggregated amyloid beta (Aβ) and hyperphosphorylated tau along with a slow decline in cognitive functions. Unlike advanced AD, the initial steps of AD pathophysiology have been poorly investigated, partially due to limited availability of animal models focused on the early, plaque-free stages of the disease. The aim of this study was to evaluate the early behavioral, anatomical and molecular alterations in wild-type rats following intracerebroventricular injections of human Aβ oligomers (AβOs). Bioactive human AD and nondemented control brain tissue extracts were characterized using ELISA and proteomics approaches. Following a bilateral infusion, rats underwent behavioral testing, including the elevated plus maze, social recognition test, Morris water maze and Y-maze within 6 weeks postinjection. An analysis of brain structure was performed with manganese-enhanced MRI. Collected brain tissues were analyzed using stereology, immunohistochemistry, ELISA and qPCR. No sensorimotor deficits affecting motor performance on different maze tasks were observed, nor was spatial memory disturbed in AD rats. In contrast, a significant impairment of social memory became evident at 21 days postinjection. This deficit was associated with a significantly decreased volume of the lateral entorhinal cortex and a tendency toward a decrease in the total brain volume. Significant increase of cleaved caspase-3-positive cells, microglial activation and proinflammatory responses accompanied by altered expression of synaptic markers were observed in the hippocampus of AD rats with immunohistochemical and qPCR approaches at 6 weeks postinjection. Our data suggest that the social memory impairment observed in AβO-injected rats might be determined by neuroinflammatory responses and synaptopathy. An infusion of native oligomeric Aβ in the rat brain represents a feasible tool to model early plaque-free events associated with AD.

Novel research on Neuroprotective effect of Bacopa monnieri L. against propionic acid induced investigation on autism in Sprague Dawley rat

Autism spectrum disorder (ASD) is characterized by complex behavioral and memory impairments resulting from abnormal brain development. The research objective is to identify the lack of understanding of the etiology of autism. The Ayurvedic system of medicine recognizes Bacopa monnieri for their potential nootropic activity to maximize brain and neuronal processes such as learning and memory. Brahmi, Bacopa monnieri has been demonstrated in Ayurvedic preparation as memory booster medicine. The neuroprotective properties of hydroalcoholic extract of Bacopa monnieri against propionic acid-induced neuroprotective effect in autistic rat models were investigated in the present study. The animal species used in the study are adult Sprague Dawley rats of both sexes were divided into four groups and administered the vehicle/extract for 28 days. Between the 22nd and 28th days of the trial, autism was caused by an intracerebroventricular infusion of propionic acid. Rats were treated to the fundamental methods such as different in vivo behavior and memory evaluation procedures during this infusion period, including the actophotometer test and the Morris water maze test. Animals were euthanized on the 29th day of the investigation to obtain brain material. Extracted brain tissues were used to calculate levels of neuroinflammatory markers (TNF-) and histological examination.

A Chinese multi-modal neuroimaging data release for increasing diversity of human brain mapping

The big-data use is becoming a standard practice in the neuroimaging field through data-sharing initiatives. It is important for the community to realize that such open science effort must protect personal, especially facial information when raw neuroimaging data are shared. An ideal tool for the face anonymization should not disturb subsequent brain tissue extraction and further morphological measurements. Using the high-resolution head images from magnetic resonance imaging (MRI) of 215 healthy Chinese, we discovered and validated a template effect on the face anonymization. Improved facial anonymization was achieved when the Chinese head templates but not the Western templates were applied to obscure the faces of Chinese brain images. This finding has critical implications for international brain imaging data-sharing. To facilitate the further investigation of potential culture-related impacts on and increase diversity of data-sharing for the human brain mapping, we released the 215 Chinese multi-modal MRI data into a database for imaging Chinese young brains, namely’I See your Brains (ISYB)’, to the public via the Science Data Bank (https://doi.org/10.11922/sciencedb.00740).