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Fulltext Neuroinflammation: A Common Pathway in Alzheimer's Disease and Epilepsy

Liew Y, Retinasamy T, Arulsamy A, Ali I, Jones NC, O'Brien TJ, et al.

J Alzheimers Dis, 2023;94(s1):S253-S265.
PMID: 37092226 DOI: 10.3233/JAD-230059

BACKGROUND: Neuroinflammation is an innate immunological response of the central nervous system that may be induced by a brain insult and chronic neurodegenerative conditions. Recent research has shown that neuroinflammation may contribute to the initiation of Alzheimer's disease (AD) pathogenesis and associated epileptogenesis.
OBJECTIVE: This systematic review aimed to investigate the available literature on the shared molecular mechanisms of neuroinflammation in AD and epilepsy.
METHODS: The search included in this systematic review was obtained from 5 established databases. A total of 2,760 articles were screened according to inclusion criteria. Articles related to the modulation of the inflammatory biomarkers commonly associated with the progression of AD and epilepsy in all populations were included in this review.
RESULTS: Only 7 articles met these criteria and were chosen for further analysis. Selected studies include both in vitro and in vivo research conducted on rodents. Several neuroinflammatory biomarkers were reported to be involved in the cross-talk between AD and epilepsy.
CONCLUSION: Neuroinflammation was directly associated with the advancement of AD and epilepsy in populations compared to those with either AD or epilepsy. However, more studies focusing on common inflammatory biomarkers are required to develop standardized monitoring guidelines to prevent the manifestation of epilepsy and delay the progression of AD in patients.

Matched MeSH terms: Brain/pathology
Numerical investigation of treated brain glioma model using a two-stage successive over-relaxation method

Hussain A, Muthuvalu MS, Faye I, Zafar M, Inc M, Afzal F, et al.

Comput Biol Med, 2023 Feb;153:106429.
PMID: 36587570 DOI: 10.1016/j.compbiomed.2022.106429

A brain tumor is a dynamic system in which cells develop rapidly and abnormally, as is the case with most cancers. Cancer develops in the brain or inside the skull when aberrant and odd cells proliferate in the brain. By depriving the healthy cells of leisure, nutrition, and oxygen, these aberrant cells eventually cause the healthy cells to perish. This article investigated the development of glioma cells in treating brain tumors. Mathematically, reaction-diffusion models have been developed for brain glioma growth to quantify the diffusion and proliferation of the tumor cells within brain tissues. This study presents the formulation the two-stage successive over-relaxation (TSSOR) algorithm based on the finite difference approximation for solving the treated brain glioma model to predict glioma cells in treating the brain tumor. Also, the performance of TSSOR method is compared to the Gauss-Seidel (GS) and two-stage Gauss-Seidel (TSGS) methods in terms of the number of iterations, the amount of time it takes to process the data, and the rate at which glioma cells grow the fastest. The implementation of the TSSOR, TSGS, and GS methods predicts the growth of tumor cells under the treatment protocol. The results show that the number of glioma cells decreased initially and then increased gradually by the next day. The computational complexity analysis is also used and concludes that the TSSOR method is faster compared to the TSGS and GS methods. According to the results of the treated glioma development model, the TSSOR approach reduced the number of iterations by between 8.0 and 71.95%. In terms of computational time, the TSSOR approach is around 1.18-76.34% faster than the TSGS and GS methods.

Matched MeSH terms: Brain/pathology
Henipavirus encephalitis

Abdullah S, Tan CT

Handb Clin Neurol, 2014;123:663-70.
PMID: 25015510 DOI: 10.1016/B978-0-444-53488-0.00032-8
Matched MeSH terms: Brain/pathology
Intracranial hypoglossal neurinomas. A report of two cases

Arumugasamay N, Sarvananthan K, Rudralingam V, Pillay RP

Med J Malaya, 1972 Mar;26(3):168-72.
PMID: 5031011
Matched MeSH terms: Brain/pathology
Fulltext A case report of near-missed heat stroke

Yeoh CW, Law WC

Medicine (Baltimore), 2023 Dec 22;102(51):e36676.
PMID: 38134114 DOI: 10.1097/MD.0000000000036676

RATIONALE: Heat-related illnesses have protean manifestations that can mimic other life-threatening conditions. The diagnosis of heat stroke requires a high index of suspicion if the patient has been exposed to a high-temperature environment. Central nervous system dysfunction is a cardinal feature. Strict adherence to temperature criteria can potentially lead to misdiagnosis.
PATIENT CONCERNS: A 37-year-old construction worker was brought in by his wife and coworker due to a sudden loss of consciousness while resting after completing his work.
DIAGNOSES: Due to challenges faced during the coronavirus disease 2019 pandemic, as well as language barriers, a detailed history from the coworker who witnessed the patient's altered sensorium was not available. He was initially suspected of having encephalitis and brainstem stroke. However, subsequent investigations revealed multiorgan dysfunction with a normal brain computed tomography and cerebral computed tomography angiogram. In view of the multiple risk factors for heat stroke, pupillary constriction, and urine color suggestive of rhabdomyolysis, a diagnosis of heat stroke was made.
INTERVENTIONS: Despite delayed diagnosis, the patient's multiorgan dysfunction recovered within days with basic supportive care.
OUTCOMES: There were no noticeable complications on follow-up 14 months later.
LESSONS: Heat stroke can be easily confused with other neurological pathologies, particularly if no history can be obtained from the patient or informant. When approaching a comatose patient, we propose that serum creatinine kinase should be considered as an initial biochemical screening test.

Matched MeSH terms: Brain/pathology
Blood-brain Barrier and Neurovascular Unit Dysfunction in Parkinson's Disease: From Clinical Insights to Pathogenic Mechanisms and Novel Therapeutic Approaches

Khor SLQ, Ng KY, Koh RY, Chye SM

CNS Neurol Disord Drug Targets, 2024;23(3):315-330.
PMID: 36999187 DOI: 10.2174/1871527322666230330093829

The blood-brain barrier (BBB) plays a crucial role in the central nervous system by tightly regulating the influx and efflux of biological substances between the brain parenchyma and peripheral circulation. Its restrictive nature acts as an obstacle to protect the brain from potentially noxious substances such as blood-borne toxins, immune cells, and pathogens. Thus, the maintenance of its structural and functional integrity is vital in the preservation of neuronal function and cellular homeostasis in the brain microenvironment. However, the barrier's foundation can become compromised during neurological or pathological conditions, which can result in dysregulated ionic homeostasis, impaired transport of nutrients, and accumulation of neurotoxins that eventually lead to irreversible neuronal loss. Initially, the BBB is thought to remain intact during neurodegenerative diseases, but accumulating evidence as of late has suggested the possible association of BBB dysfunction with Parkinson's disease (PD) pathology. The neurodegeneration occurring in PD is believed to stem from a myriad of pathogenic mechanisms, including tight junction alterations, abnormal angiogenesis, and dysfunctional BBB transporter mechanism, which ultimately causes altered BBB permeability. In this review, the major elements of the neurovascular unit (NVU) comprising the BBB are discussed, along with their role in the maintenance of barrier integrity and PD pathogenesis. We also elaborated on how the neuroendocrine system can influence the regulation of BBB function and PD pathogenesis. Several novel therapeutic approaches targeting the NVU components are explored to provide a fresh outlook on treatment options for PD.

Matched MeSH terms: Brain/pathology
The past, present and future of imaging in multiple sclerosis

Ramli N, Rahmat K, Azmi K, Chong HT

J Clin Neurosci, 2010 Apr;17(4):422-7.
PMID: 20167498 DOI: 10.1016/j.jocn.2009.09.014

Despite technological advances in imaging, multiple sclerosis (MS) remains a clinical diagnosis that is supported, but not replaced, by laboratory or imaging findings. However, imaging is essential in the current diagnostic criteria of MS, for prediction of the likelihood of MS for patients with clinically isolated syndromes, correlation with lesion pathology and assessment of treatment outcome. This article gives an overview of imaging in MS with particular emphasis on the role of MRI in various diagnostic imaging criteria. Novel imaging for MS using 3 Tesla field strengths, magnetization transfer imaging, diffusion tensor imaging, magnetic resonance spectroscopy and cell-specific contrast will be reviewed.

Matched MeSH terms: Brain/pathology
Biology and pathogenesis of Naegleria fowleri

Siddiqui R, Ali IK, Cope JR, Khan NA

Acta Trop, 2016 Dec;164:375-394.
PMID: 27616699 DOI: 10.1016/j.actatropica.2016.09.009

Naegleria fowleri is a protist pathogen that can cause lethal brain infection. Despite decades of research, the mortality rate related with primary amoebic meningoencephalitis owing to N. fowleri remains more than 90%. The amoebae pass through the nose to enter the central nervous system killing the host within days, making it one of the deadliest opportunistic parasites. Accordingly, we present an up to date review of the biology and pathogenesis of N. fowleri and discuss needs for future research against this fatal infection.

Matched MeSH terms: Brain/pathology
Multiple sclerosis. The neuropathology of a case with a plea

Arumugasamy N

Med J Malaya, 1969 Sep;24(1):45-8.
PMID: 4243843
Matched MeSH terms: Brain/pathology*
Fulltext Management of acute intracerebral haemorrhage - an update

Law ZK, Appleton JP, Bath PM, Sprigg N

Clin Med (Lond), 2017 Apr;17(2):166-172.
PMID: 28365631 DOI: 10.7861/clinmedicine.17-2-166

Managing acute intracerebral haemorrhage is a challenging task for physicians. Evidence shows that outcome can be improved with admission to an acute stroke unit and active care, including urgent reversal of anticoagulant effects and, potentially, intensive blood pressure reduction. Nevertheless, many management issues remain controversial, including the use of haemostatic therapy, selection of patients for neurosurgery and neurocritical care, the extent of investigations for underlying causes and the benefit versus risk of restarting antithrombotic therapy after an episode of intracerebral haemorrhage.

Matched MeSH terms: Brain/pathology
Blood-based therapies to combat neurodegenerative diseases

Lee JY, Lim MCX, Koh RY, Tsen MT, Chye SM

Metab Brain Dis, 2024 Jun;39(5):985-1004.
PMID: 38842660 DOI: 10.1007/s11011-024-01368-x

Neurodegeneration, known as the progressive loss of neurons in terms of their structure and function, is the principal pathophysiological change found in the majority of brain-related disorders. Ageing has been considered the most well-established risk factor in most common neurodegenerative diseases, such as Parkinson's disease (PD) and Alzheimer's disease (AD). There is currently no effective treatment or cure for these diseases; the approved therapeutic options to date are only for palliative care. Ageing and neurodegenerative diseases are closely intertwined; reversing the aspects of brain ageing could theoretically mitigate age-related neurodegeneration. Ever since the regenerative properties of young blood on aged tissues came to light, substantial efforts have been focused on identifying and characterizing the circulating factors in the young and old systemic milieu that may attenuate or accentuate brain ageing and neurodegeneration. Later studies discovered the superiority of old plasma dilution in tissue rejuvenation, which is achieved through a molecular reset of the systemic proteome. These findings supported the use of therapeutic blood exchange for the treatment of degenerative diseases in older individuals. The first objective of this article is to explore the rejuvenating properties of blood-based therapies in the ageing brains and their therapeutic effects on AD. Then, we also look into the clinical applications, various limitations, and challenges associated with blood-based therapies for AD patients.

Matched MeSH terms: Brain/pathology
Classification of Alzheimer disease using DenseNet-201 based on deep transfer learning technique

Zia-Ur-Rehman, Awang MK, Rashid J, Ali G, Hamid M, Mahmoud SF, et al.

PLoS One, 2024;19(9):e0304995.
PMID: 39240975 DOI: 10.1371/journal.pone.0304995

Alzheimer's disease (AD) is a brain illness that causes gradual memory loss. AD has no treatment and cannot be cured, so early detection is critical. Various AD diagnosis approaches are used in this regard, but Magnetic Resonance Imaging (MRI) provides the most helpful neuroimaging tool for detecting AD. In this paper, we employ a DenseNet-201 based transfer learning technique for diagnosing different Alzheimer's stages as Non-Demented (ND), Moderate Demented (MOD), Mild Demented (MD), Very Mild Demented (VMD), and Severe Demented (SD). The suggested method for a dataset of MRI scans for Alzheimer's disease is divided into five classes. Data augmentation methods were used to expand the size of the dataset and increase DenseNet-201's accuracy. It was found that the proposed strategy provides a very high classification accuracy. This practical and reliable model delivers a success rate of 98.24%. The findings of the experiments demonstrate that the suggested deep learning approach is more accurate and performs well compared to existing techniques and state-of-the-art methods.

Matched MeSH terms: Brain/pathology
Melkersson-Rosenthal syndrome with involvement of masticatory muscles

Kuok SS, Ramli N, Tan CT, Goh KJ

Clin Neurol Neurosurg, 2015 Mar;130:8-10.
PMID: 25562719 DOI: 10.1016/j.clineuro.2014.12.003
Matched MeSH terms: Brain/pathology*
Neuronavigation with the universal probe to access intracranial targets

Waran V, Chandran H, Devaraj P, Ravindran K, Rathinam AK, Balakrishnan YK, et al.

J Neurol Surg A Cent Eur Neurosurg, 2014 Nov;75(6):422-6.
PMID: 23955263 DOI: 10.1055/s-0033-1345091

The universal probe is a tool devised to allow navigation-directed biopsies and drainage procedures to be performed in a simple manner using a single hardware and software.

Matched MeSH terms: Brain/pathology
Automatic white matter lesion segmentation using an adaptive outlier detection method

Ong KH, Ramachandram D, Mandava R, Shuaib IL

Magn Reson Imaging, 2012 Jul;30(6):807-23.
PMID: 22578927 DOI: 10.1016/j.mri.2012.01.007

White matter (WM) lesions are diffuse WM abnormalities that appear as hyperintense (bright) regions in cranial magnetic resonance imaging (MRI). WM lesions are often observed in older populations and are important indicators of stroke, multiple sclerosis, dementia and other brain-related disorders. In this paper, a new automated method for WM lesions segmentation is presented. In the proposed method, the presence of WM lesions is detected as outliers in the intensity distribution of the fluid-attenuated inversion recovery (FLAIR) MR images using an adaptive outlier detection approach. Outliers are detected using a novel adaptive trimmed mean algorithm and box-whisker plot. In addition, pre- and postprocessing steps are implemented to reduce false positives attributed to MRI artifacts commonly observed in FLAIR sequences. The approach is validated using the cranial MRI sequences of 38 subjects. A significant correlation (R=0.9641, P value=3.12×10(-3)) is observed between the automated approach and manual segmentation by radiologist. The accuracy of the proposed approach was further validated by comparing the lesion volumes computed using the automated approach and lesions manually segmented by an expert radiologist. Finally, the proposed approach is compared against leading lesion segmentation algorithms using a benchmark dataset.

Matched MeSH terms: Brain/pathology*
Brain biometals and Alzheimer's disease - boon or bane?

Prakash A, Dhaliwal GK, Kumar P, Majeed AB

Int J Neurosci, 2017 Feb;127(2):99-108.
PMID: 27044501

Alzheimer's disease (AD) is the most common form of dementia. Several hypotheses have been put forward to explain the basis of disease onset and progression. A complicated array of molecular events has been implicated in the pathogenesis of AD. It is attributed to a variety of pathological conditions that share similar critical processes, such as oxidative stress, proteinaceous aggregations, mitochondrial dysfunctions and energy failure. There is increasing evidence suggesting that metal homeostasis is dysregulated in the pathology of AD. Biometals play an important role in the normal body functioning but AD may be mediated or triggered by disproportion of metal ions leading to changes in critical biological systems and initiating a cascade of events finally leading to neurodegeneration and cell death. The link is multifactorial, and although the source of the shift in oxidative homeostasis is still unclear, current evidence points to changes in the balance of redox transition metals, especially iron, copper (Cu) and other trace metals. Their levels in the brain are found to be elevated in AD. In other neurodegenerative disorders, Cu, zinc, aluminum and manganese are involved. This paper is a review of recent advances of the role of metals in the pathogenesis and pathophysiology of AD and related neurodegenerative diseases.

Matched MeSH terms: Brain/pathology
Fulltext The metastable brain associated with autistic-like traits of typically developing individuals

Sase T, Kitajo K

PLoS Comput Biol, 2021 04;17(4):e1008929.
PMID: 33861737 DOI: 10.1371/journal.pcbi.1008929

Metastability in the brain is thought to be a mechanism involved in the dynamic organization of cognitive and behavioral functions across multiple spatiotemporal scales. However, it is not clear how such organization is realized in underlying neural oscillations in a high-dimensional state space. It was shown that macroscopic oscillations often form phase-phase coupling (PPC) and phase-amplitude coupling (PAC), which result in synchronization and amplitude modulation, respectively, even without external stimuli. These oscillations can also make spontaneous transitions across synchronous states at rest. Using resting-state electroencephalographic signals and the autism-spectrum quotient scores acquired from healthy humans, we show experimental evidence that the PAC combined with PPC allows amplitude modulation to be transient, and that the metastable dynamics with this transient modulation is associated with autistic-like traits. In individuals with a longer attention span, such dynamics tended to show fewer transitions between states by forming delta-alpha PAC. We identified these states as two-dimensional metastable states that could share consistent patterns across individuals. Our findings suggest that the human brain dynamically organizes inter-individual differences in a hierarchy of macroscopic oscillations with multiple timescales by utilizing metastability.

Matched MeSH terms: Brain/pathology
The Mechanism of Action of Salsolinol in Brain: Implications in Parkinson's Disease

Voon SM, Ng KY, Chye SM, Ling APK, Voon KGL, Yap YJ, et al.

CNS Neurol Disord Drug Targets, 2020;19(10):725-740.
PMID: 32881676 DOI: 10.2174/1871527319666200902134129

1-Methyl-1,2,3,4-tetrahydroisoquinoline-6,7-diol, commonly known as salsolinol, is a compound derived from dopamine. It was first discovered in 1973 and has gained attention for its role in Parkinson's disease. Salsolinol and its derivatives were claimed to play a role in the pathogenesis of Parkinson's disease as a neurotoxin that induces apoptosis of dopaminergic neurons due to its structural similarity to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its ability to induce Parkinsonism. In this article, we discussed the biosynthesis, distribution and blood-brain barrier permeability of salsolinol. The roles of salsolinol in a healthy brain, particularly the interactions with enzymes, hormone and catecholamine, were reviewed. Finally, we discussed the involvement of salsolinol and its derivatives in the pathogenesis of Parkinson's disease.

Matched MeSH terms: Brain/pathology*
Fulltext Improved Method for the Establishment of an In Vitro Blood-Brain Barrier Model Based on Porcine Brain Endothelial Cells

Nielsen SSE, Siupka P, Georgian A, Preston JE, Tóth AE, Yusof SR, et al.

J Vis Exp, 2017 09 24.
PMID: 28994773 DOI: 10.3791/56277

The aim of this protocol presents an optimized procedure for the purification and cultivation of pBECs and to establish in vitro blood-brain barrier (BBB) models based on pBECs in mono-culture (MC), MC with astrocyte-conditioned medium (ACM), and non-contact co-culture (NCC) with astrocytes of porcine or rat origin. pBECs were isolated and cultured from fragments of capillaries from the brain cortices of domestic pigs 5-6 months old. These fragments were purified by careful removal of meninges, isolation and homogenization of grey matter, filtration, enzymatic digestion, and centrifugation. To further eliminate contaminating cells, the capillary fragments were cultured with puromycin-containing medium. When 60-95% confluent, pBECs growing from the capillary fragments were passaged to permeable membrane filter inserts and established in the models. To increase barrier tightness and BBB characteristic phenotype of pBECs, the cells were treated with the following differentiation factors: membrane permeant 8-CPT-cAMP (here abbreviated cAMP), hydrocortisone, and a phosphodiesterase inhibitor, RO-20-1724 (RO). The procedure was carried out over a period of 9-11 days, and when establishing the NCC model, the astrocytes were cultured 2-8 weeks in advance. Adherence to the described procedures in the protocol has allowed the establishment of endothelial layers with highly restricted paracellular permeability, with the NCC model showing an average transendothelial electrical resistance (TEER) of 1249 ± 80 Ω cm2, and paracellular permeability (Papp) for Lucifer Yellow of 0.90 10-6 ± 0.13 10-6 cm sec-1 (mean ± SEM, n=55). Further evaluation of this pBEC phenotype showed good expression of the tight junctional proteins claudin 5, ZO-1, occludin and adherens junction protein p120 catenin. The model presented can be used for a range of studies of the BBB in health and disease and, with the highly restrictive paracellular permeability, this model is suitable for studies of transport and intracellular trafficking.

Matched MeSH terms: Brain/pathology*
Mapping cerebral atrophy and hypometabolism on 18F-FDG PET/CT scans for detecting Alzheimer's disease in the Malaysian population using a Malaysian brain atlas template

Siti Aishah AA, Normala I, Faruque Reza M, M Iqbal S

Med J Malaysia, 2023 Jan;78(1):46-53.
PMID: 36715191

INTRODUCTION: Studies are lacking in evaluating brain atrophy patterns in the Malaysian population. This study aimed to compare the patterns of cerebral atrophy and impaired glucose metabolism on 18F-FDG PET/CT imaging in various stages of AD in a Klang Valley population by using voxelbased morphometry in SPM12.
MATERIALS AND METHODS: 18F-FDG PET/CT images of 14 healthy control (HC) subjects (MoCA score > 26 (mean+SD~ 26.93+0.92) with no clinical evidence of cognitive deficits or neurological disease) and 16 AD patients (MoCA ≤22 (mean+SD~18.6+9.28)) were pre-processed in SPM12 while using our developed Malaysian healthy control brain template. The AD patients were assessed for disease severity using ADAS-Cog neuropsychological test. KNE96 template was used for registration-induced deformation in comparison with the ICBM templates. All deformation fields were corrected using the Malaysian healthy control template. The images were then nonlinearly modified by DARTEL to segment grey matter (GM), white matter (WM) and cerebrospinal fluid (CSF) to produce group-specific templates. Age, intracranial volume, MoCA score, and ADASCog score were used as variables in two sample t test between groups. The inference of our brain analysis was based on a corrected threshold of p<0.001 using Z-score threshold of 2.0, with a positive value above it as hypometabolic. The relationship between regional atrophy in GM and WM atrophy were analysed by comparing the means of cortical thinning between normal control and three AD stages in 15 clusters of ROI based on Z-score less than 2.0 as atrophied.
RESULTS: One-way ANOVA indicated that the means were equal for TIV, F(2,11) = 1.310, p=0.309, GMV, F(2,11) = 0.923, p=0.426, WMV, F(2,11) = 0.158, p=0.856 and CSF, F(2,11) = 1.495 p=0.266. Pearson correlations of GM, WM and CSF volume between HC and AD groups indicated the presence of brain atrophy in GM (p=-0.610, p<0.0001), WM (p=-0.178, p=0.034) and TIV (p=-0.374, p=0.042) but showed increased CSF volume (p=0.602, p<0.0001). Voxels analysis of the 18FFDG PET template revealed that GM atrophy differs significantly between healthy control and AD (p<0.0001). Zscore comparisons in the region of GM & WM were shown to distinguish AD patients from healthy controls at the prefrontal cortex and parahippocampal gyrus. The atrophy rate within each ROI is significantly different between groups (c2=35.9021, df=3, p<0.0001), Wilcoxon method test showed statistically significant differences were observed between Moderate vs. Mild AD (p<0.0001), Moderate AD vs. healthy control (p=0.0005), Mild AD vs. HC (p=0.0372) and Severe AD vs. Moderate AD (p<0.0001). The highest atrophy rate within each ROI between the median values ranked as follows severe AD vs. HC (p<0.0001) > mild AD vs. HC (p=0.0091) > severe AD vs. moderate AD (p=0.0143).
CONCLUSION: We recommend a reliable method in measuring the brain atrophy and locating the patterns of hypometabolism using a group-specific template registered to a quantitatively validated KNE96 group-specific template. The studied regions together with neuropsychological test approach is an effective method for the determination of AD severity in a Malaysian population.

Matched MeSH terms: Brain/pathology

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