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Fulltext Anti-cholinesterase, anti-inflammatory and antioxidant properties of Combretum micranthum G. Don: Potential implications in neurodegenerative disease

Kpemissi M, Kantati YT, Veerapur VP, Eklu-Gadegbeku K, Hassan Z

IBRO Neurosci Rep, 2023 Jun;14:21-27.
PMID: 36578633 DOI: 10.1016/j.ibneur.2022.12.001

BACKGROUND: Brain damage is a severe and common pathology that leads to life-threatening diseases. Despite development in the research, the medical evidence of the effectiveness of potential neuroprotective medicines is insufficient. As a result, there is an immense and urgent demand for promising medication. For millennia, herbal remedies were a fundamental aspect of medical treatments. Combretum micranthum (CM), a plant of the family Combretaceae in sub-Saharan Africa, has been utilized in folklore medicine to cure diverse human ailments. In order to develop a neuroprotective phytomedicine, the current research was undertaken to explore the antioxidant, anti-inflammatory, anticholinesterase and neuroprotective potential of CM extract.
METHODS: Colorimetric methods were used to determine CM antioxidant activity, in-vitro protein denaturation and membrane destabilization assays were used to evaluate its anti-inflammatory capacity, anticholinesterase activity was carried out using Ellman's method, and neuroprotective potential was assessed on brain homogenate stressed with ferric chloride and ascorbic acid (FeCl2-AA) by assessing the lipoperoxidation biomarker malondialdehyde (MDA).
RESULTS: In Ferric Reducing Antioxidant Power (IC50 = 27.15 ± 0.06 µg/mL) and Total Antioxidant Capacity (IC50 = 31.13 ± 0.02 µg/mL), CM extract demonstrated strong antioxidant activity. Anti-inflammatory effect were improved in heat-induced Egg albumin and BSA denaturation (IC 50 = 46.35 ± 1.53 and 23.94 ± 1.10 µg/mL) as well as heat and hypotonia induced membrane destabilization (IC 50 = 20.96 ± 0.11 and 16.75 ± 0.94 µg/mL).CM extract showed strong anticholinesterase activity (IC 50 = 59.85 ± 0.91 µg/mL). In an ex-vivo neuroprotective model, CM extract showed substantial inhibition (p
Fulltext Neurodegeneration and inflammation crosstalk: Therapeutic targets and perspectives

Mohamed W, Kumar J, Alghamdi BS, Soliman AH, Toshihide Y

IBRO Neurosci Rep, 2023 Jun;14:95-110.
PMID: 37388502 DOI: 10.1016/j.ibneur.2022.12.003

Glia, which was formerly considered to exist just to connect neurons, now plays a key function in a wide range of physiological events, including formation of memory, learning, neuroplasticity, synaptic plasticity, energy consumption, and homeostasis of ions. Glial cells regulate the brain's immune responses and confers nutritional and structural aid to neurons, making them an important player in a broad range of neurological disorders. Alzheimer's, ALS, Parkinson's, frontotemporal dementia (FTD), and epilepsy are a few of the neurodegenerative diseases that have been linked to microglia and astroglia cells, in particular. Synapse growth is aided by glial cell activity, and this activity has an effect on neuronal signalling. Each glial malfunction in diverse neurodegenerative diseases is distinct, and we will discuss its significance in the progression of the illness, as well as its potential for future treatment.
Fulltext Integrating nutriepigenomics in Parkinson's disease management: New promising strategy in the omics era

Razali K, Algantri K, Loh SP, Cheng SH, Mohamed W

IBRO Neurosci Rep, 2022 Dec;13:364-372.
PMID: 36590101 DOI: 10.1016/j.ibneur.2022.10.003

Parkinson's disease (PD) is the most prevalent brain motor disorder and is frequently regarded as an idiopathic and sporadic disease due to its unclear etiology. Although the pathological mechanisms of PD have already been investigated at various omics levels, no disease-modifying drugs are currently available. At the moment, treatments can only provide symptomatic relief to control or improve motor symptoms. Parkinson's disease is a multifactorial disease, the development and progression of which are influenced by multiple factors, including the genetic markups and the environment. As an indispensable component of our daily life, nutrition is considered one of the most robust environmental factors affecting our health. Consequently, depending on our dietary habits, nutrition can either induce or reduce our susceptibility to PD. Epigenetic mechanisms regulate gene expression through DNA methylation, histone modifications, and non-coding RNAs (ncRNAs) activity. Accumulating evidence from nutriepigenomics studies has reported altered epigenetic mechanisms in clinical and pre-clinical PD models, and the potential role of nutrition in modifying the changes. In addition, through nutrigenetics and nutrigenomics studies, the diet-gene, and gene-diet interactions concerning PD development and progression have been investigated. Herein, current findings on the roles of nutrition in epigenetic mechanisms underpinning PD development and progression are discussed. Recent advancements in the multi-omics approach in PD nutrition research are also underlined. The ability of nutrients to influence epigenetic mechanisms and the availability of multi-omics applications compel the immediate use of personalized nutrition as adjuvant therapy for PD.
Fulltext Mitochondria dysfunction and bipolar disorder: From pathology to therapy

Lam XJ, Xu B, Yeo PL, Cheah PS, Ling KH

IBRO Neurosci Rep, 2023 Jun;14:407-418.
PMID: 37388495 DOI: 10.1016/j.ibneur.2023.04.002

Bipolar disorder (BD) is one of the major psychiatric diseases in which the impairment of mitochondrial functions has been closely connected or associated with the disease pathologies. Different lines of evidence of the close connection between mitochondria dysfunction and BD were discussed with a particular focus on (1) dysregulation of energy metabolism, (2) effect of genetic variants, (3) oxidative stress, cell death and apoptosis, (4) dysregulated calcium homeostasis and electrophysiology, and (5) current as well as potential treatments targeting at restoring mitochondrial functions. Currently, pharmacological interventions generally provide limited efficacy in preventing relapses or recovery from mania or depression episodes. Thus, understanding mitochondrial pathology in BD will lead to novel agents targeting mitochondrial dysfunction and formulating new effective therapy for BD.
Fulltext Neural fate commitment of rat full-term amniotic fluid stem cells via three-dimensional embryoid bodies and neurospheres formation

Azmi N, Mustaffa Al Bakri SS, Khor W, Hamzah SN, Ferdaos N, Ling KH, et al.

IBRO Neurosci Rep, 2023 Jun;14:235-243.
PMID: 37388489 DOI: 10.1016/j.ibneur.2023.01.003

Full-term amniotic fluid stem cell (AFSC) is an underexplored reserve of broadly multipotent stem cells with potential applications in cell replacement therapy. One aspect worth exploring is the potential of AFSCs to differentiate into neural lineages. Previously, we have shown that full-term AFSC lines established from term gestation amniotic fluid, known as R3 and R2, differentiated into neural lineage through the monolayer adherent method suggesting their neurogenic potential. The neural commitment of the cells through the formation of multicellular aggregates has never been shown before. Here, we explored the ability of R3 to commit to neural fate via the formation of three-dimensional multicellular aggregates, namely embryoid bodies (EBs) and neurospheres, exhibiting distinct characteristics resembling EBs and neurospheres as obtained from other published pluripotent and neural stem cells (NSCs), respectively. Different cell seeding densities of the cells cultured in their respective induction medium generated two distinct types of aggregates with the appropriate sizes for EBs (300-350 µm) and neurospheres (50-100 µm). The neurospheres expressed a significantly high level of Nestin than EBs. However, EBs stained positive for TUJ1, suggesting the presence of early post-mitotic neurons representing the ectodermal lineage. In contrast, the presence of the NSC population in neurosphere culture was validated with positive expression of Sox1. Notably, dissociated cells from both aggregates differentiated into MAP2-positive neural cells, highlighting the ability of both types of multicellular aggregates to commit to the neural fate. In conclusion, this study highlights the first evidence of neurosphere formation from full-term AFSCs in addition to neural fate commitment via EBs formation. Findings from this study allow researchers to select the suitable approach for neural cell generation and expansion according to research needs.
Fulltext Is cerebral small vessel disease a central nervous system interstitial fluidopathy?

Abdul Hamid H, Hambali A, Okon U, Che Mohd Nassir CMN, Mehat MZ, Norazit A, et al.

IBRO Neurosci Rep, 2024 Jun;16:98-105.
PMID: 39007087 DOI: 10.1016/j.ibneur.2023.12.004

A typical anatomical congregate and functionally distinct multicellular cerebrovascular dynamic confer diverse blood-brain barrier (BBB) and microstructural permeabilities to conserve the health of brain parenchymal and its microenvironment. This equanimity presupposes the glymphatic system that governs the flow and clearance of metabolic waste and interstitial fluids (ISF) through venous circulation. Following the introduction of glymphatic system concept, various studies have been carried out on cerebrospinal fluid (CSF) and ISF dynamics. These studies reported that the onset of multiple diseases can be attributed to impairment in the glymphatic system, which is newly referred as central nervous system (CNS) interstitial fluidopathy. One such condition includes cerebral small vessel disease (CSVD) with poorly understood pathomechanisms. CSVD is an umbrella term to describe a chronic progressive disorder affecting the brain microvasculature (or microcirculation) involving small penetrating vessels that supply cerebral white and deep gray matter. This review article proposes CSVD as a form of "CNS interstitial fluidopathy". Linking CNS interstitial fluidopathy with CSVD will open a better insight pertaining to the perivascular space fluid dynamics in CSVD pathophysiology. This may lead to the development of treatment and therapeutic strategies to ameliorate the pathology and adverse effect of CSVD.
Challenges of status epilepticus management in a resource-limited setting: A review

Lim KS, Fong SL, Yahaya SN, Thuy Le MA, Khosama H

IBRO Neurosci Rep, 2024 Dec;17:83-86.
PMID: 39026897 DOI: 10.1016/j.ibneur.2024.06.001

Status epilepticus (SE) is a life-threatening neurological condition with significant mortality. Rapid management is essential to minimize the mortality and disability of SE. Two recent trials provided evidence to guide SE management in early and established stages. The Rapid Anticonvulsant Medication Prior To Arrival Trial (RAMPART, 2011) showed that intramuscular midazolam is a better alternative for early convulsive SE in prehospital settings. The Established Status Epilepticus Treatment Trial (ESETT, 2020) supported the use of sodium valproate and levetiracetam as second-line treatment for its efficacy and shorter administration time. However, there are challenges to revising the status epilepticus management in resource-limited settings, in pre-hospital, first- and second-line treatment, as well as management of refractory and super-refractory SE. These challenges included restrictions or lack of training in the administration of benzodiazepine in the prehospital setting, limited availability and accessibility of newer antiseizure medications (ASMs) in emergency departments and smaller hospitals, and low clinicians' awareness of the latest evidence. A collaborative effort to educate, improve awareness, and make certain ASMs more readily available is recommended to achieve a better clinical outcome in SE.