Central nervous system diseases associated with blood brain barrier breakdown - A Comprehensive update of existing literatures

Abstract

Blood vessels that supply and feed the central nervous system (CNS) possess unique and exclusive properties, named as blood–brain barrier (BBB). It is responsible for tight regulation of the movement of ions, molecules, and cells between the blood and the brain thereby maintaining controlled chemical composition of the neuronal milieu required for appropriate functioning. It also protects the neural tissue from toxic plasma components, blood cells and pathogens from entering the brain. In this review the importance of BBB and its disruption causing brain pathology and progression to different neurological diseases like Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD) etc. will be discussed.

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“…The authors reported increase in blood density, reduction in blood vessel diameter and BBB leakage in both the mice model and HD patients [40]. Some other studies also reported about the evidence BBB disruption in HD [41][42][43][44]. Amyotrophic lateral sclerosis: Animal model studies have reported previously about the occurrence blood spinal cord barrier breakdown before motor neuron injury [45][46][47][48][49].…”

“…HIV-Assoc iated Neurocognitive Disorder: HIV-1positive individuals today still develop HIV-1-ass ociated dementia (HAD) and neurocognitive impairment in spite of good prognosis with antiretroviral therapy [76,77]. Imbalances between MMPs and TIMPs are involved in BBB disruption and are implicated in the pathogenesis of HAND in H IV-1 patients [78].…”

“…Post TBI astrocyte-derived vascular permeability factors including vascular endothelial growth factors, MMP, nitric oxide, glutamate and endothelin-1, enhance BBB permeability leading to BBB disruption [100]. Several biomarkers has been linked to BBB disruption like CSF/serum albumin ratio [104], tight junction proteins [105,106], S100B [107,108], Plasmasoluble prion protein (PrPc) [109,110]. https://doi.org/10.29328/journal.jnnd.1001035…”

“…The BBB is centrally positioned within the NVU and is formed by a monolayer of tightly-sealed endothelial cells along the vascular tree expressing low paracellular and transcellular permeability [8,11,12]. BBB formation during embryogenesis is complex and is dependent on various signaling molecules like VEG F [13], wnt [14],sonic hedgehog [15], platelet derived growth factor-BB-platelet derived growth factor receptor beta-signaling [16],axon guidance molecules [17] and BBB speci ic components [8]. BBB maturation and its maintenance are controlled by neuronal activity-induced vascular plasticity, microRNAs and exosomal regulation, apicobasal polarity of BBB endothelium, vascular cell lineages, immunoregulation of the BBB [18] and breakdown [19].…”

Hierarchy of pathogenetic mechanisms of chronic cerebrovascular insufficiency and therapeutic strategies for neuroprotection

“…To increase the effectiveness of therapy, it is advisable to combine neuropetides with antioxidants and antihypoxants, choline precursor drugs. В ЦНС различают 4 типа нейроглиальных клеток: астроциты, микроглиальные клетки, олигодендроциты и эпендимальные клетки [10]. Активация астроцитов при любой ишемии ускоряет процессы нейродегенерации и увеличивает зону повреждения гиппокампа, формирования глиальных рубцов с ингибирующим аксональным действием.…”