Abstract：
:Alzheimer disease (AD) is a major cause of dementia. Several mechanisms have been postulated to explain its pathogenesis, beta-amyloid (A beta toxicity, cholinergic dysfunction, Tau hyper-phosphorylation, oxidative damage, synaptic dysfunction and inflammation secondary to senile plaques, among others. Glial cells are the major producers of inflammatory mediators, and cytotoxic activation of glial cells is linked to several neurodegenerative diseases; however, whether inflammation is a consequence or the cause of neurodegeneration is still unclear. I propose that inflammation and cellular stress associated with aging are key events in the development of AD through the induction of glial dysfunction. Dysregulated inflammatory response can elicit glial cell activation by compounds which are normally poorly reactive. Inflammation can also be the major cause of defective handling of A beta and the amyloid precursor protein (APP). Here I review evidence that support the proposal that dysfunctional glia and the resulting neuroinflammation can explain many features of AD. Evidence supports the notion that damage caused by inflammation is not only a primary cause of neurodegeneration but also an inducer for the accumulation of A beta in AD. Dysfunctional glia can result in impaired neuronal function in AD, as well as in many progressive neurodegenerative disorders. We show that microglial cell activation is enhanced under pro-inflammatory conditions, indicating that glial cell responses to A beta related proteins can be critically dependent on the priming of glial cells by pro-inflammatory factors.
journal_name
Neurotox Resjournal_title
Neurotoxicity researchauthors
von Bernhardi Rdoi
10.1007/BF03033906subject
Has Abstractpub_date
2007-12-01 00:00:00pages
215-32issue
4eissn
1029-8428issn
1476-3524journal_volume
12pub_type
杂志文章,评审abstract：:Mobile phone communications are conveyed by radiofrequency (RF) electromagnetic fields, including pulse-modulated global system for mobile communications (GSM)-1800 MHz, whose effects on the CNS affected by pathological states remain to be specified. Here, we investigated whether a 2-h head-only exposure to GSM-1800 M...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-017-9756-3
更新日期：2017-10-01 00:00:00
abstract：:There has been a growing recognition of the role of neuroinflammation caused by microglia-exaggerated release of inflammatory mediators in the pathogenesis of Parkinson's disease (PD). Pituitary adenylate cyclase activating polypeptide (PACAP) is an endogenous 38 amino acid containing neuropeptide that has been shown ...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-014-9468-x
更新日期：2014-10-01 00:00:00
abstract：:Our previous investigation showed that melamine in offspring hippocampus appeared to not be the critical factor for cognitive defects. The present study was to investigate whether the cognitive impairments induced by prenatal and postnatal melamine exposure and persisted into adulthood, and to evaluate the differences...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-015-9578-0
更新日期：2016-02-01 00:00:00
abstract：:Integrin β8 is a key regulator of vascular homeostasis in brain development and in vitro studies show that β8 protects against oxygen-glucose deprivation-induced neuronal apoptosis. However, the role β8 plays in vivo in neonatal rats with hypoxic-ischemic (HI) brain injury is not known. Here, we report the function of...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-012-9312-0
更新日期：2012-11-01 00:00:00
abstract：:The deaths of neurons, astrocytes and endothelial cells have been described in patients with HIV (human immunodeficiency virus) dementia. HIV-1 does not infect neurons; instead, neurotoxic substances shed by infected glia and macrophages can induce a form of programmed cell death called apoptosis in neurons. These neu...
journal_title：Neurotoxicity research
pub_type： 杂志文章,评审
doi：10.1007/BF03033824
更新日期：2005-10-01 00:00:00
abstract：:Salsolinol (6,7-dihydroxy-1-methyl-1,2,3,4-tetrahydroisoquinoline), widely available in many edibles, is considered to alter the function of dopaminergic neurons in the central nervous system and thus, multiple hypotheses on its either physiological and/or pathophysiological role have emerged. The aim of our work was ...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-019-00118-7
更新日期：2020-02-01 00:00:00
abstract：:1-Methyl-1,2,3,4-tetrahydroisoquinoline (1MeTIQ) is present in the human and rodent brain as a mixture of stereospecific (R)- and (S)-1MeTIQ enantiomers. The racemate, (R,S)-1MeTIQ, exhibits neuroprotective activity as shown in the earlier study by the authors, and In addition, it was suggested to play a crucial physi...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-010-9228-5
更新日期：2011-08-01 00:00:00
abstract：:Asiatic acid (AA), a triterpenoid present in Centella asiatica, possesses the ability to cross blood brain barrier and received considerable attention for its neuroprotective role. We have reported the benefit of AA against aluminum chloride (AlCl3)-induced amyloid pathology, enhanced acetylcholine esterase (AChE) act...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-019-9999-2
更新日期：2019-05-01 00:00:00
abstract：:Myelin abnormalities, oligodendrocyte damage, and concomitant glia activation are common characteristics of demyelinating diseases of the central nervous system. Administration of the neurotoxicant cuprizone (CPZ) has been extensively used to establish a reproducible mouse model of demyelination. However, its effects ...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-019-00154-3
更新日期：2020-03-01 00:00:00
abstract：:Reoccurring seasonal cyanobacterial harmful algal blooms (CHABs) persist in many waters, and recent work has shown links between CHAB and elevated risk of amyotrophic lateral sclerosis (ALS). Quantifying the exposure levels of CHAB as a potential risk factor for ALS is complicated by human mobility, potential pathways...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-017-9740-y
更新日期：2018-01-01 00:00:00
abstract：:The aim of the present studies was to evaluate cocaine-induced changes in the concentrations of different redox forms of cysteine (Cys) and homocysteine (Hcy), and products of anaerobic Cys metabolism, i.e., labile, reduced sulfur (LS) in the rat plasma. The above-mentioned parameters were determined after i.p. acute ...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-013-9403-6
更新日期：2013-10-01 00:00:00
abstract：:Early-life stress is a potent risk factor for development of psychiatric conditions such as depression. The underlying mechanisms remain poorly understood. Here, we used the early-life social isolation (ESI) model of early-life stress in rats to characterize development of depressive-like behavior, the role of microgl...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-016-9696-3
更新日期：2017-05-01 00:00:00
abstract：:Iron accumulation is considered to be involved in the pathogenesis of Parkinson's disease (PD). Our previous studies have observed that Rg1, a major pharmacologically active ingredient from Ginseng, could protect dopaminergic neurons by reducing nigral iron levels through regulating the expression of iron transporters...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-012-9362-3
更新日期：2013-07-01 00:00:00
abstract：:Environmental factors and endogenously produced toxins, such as 1-benzyl-1,2,3,4-tetrahydroisoquinoline (1BnTIQ), are considered to be involved in the pathogenesis of Parkinson's disease (PD). In this study, we investigated the impact of single and multiple 1BnTIQ (25 and 50 mg/kg i.p.) administration on L-DOPA-induce...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-014-9476-x
更新日期：2014-10-01 00:00:00
abstract：:Methamphetamine (METH) is an illicit drug that is also neurotoxic. Recent studies suggest that in addition to dopamine terminal degeneration in the striatum, METH causes apoptosis in cortical neurons. Earlier, we showed that c-fos knockout mice are more susceptible to the toxic effects of the drug. In order to identif...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1080/1029842021000045453
更新日期：2002-11-01 00:00:00
abstract：:Organophosphate (OP) poisoning is associated with long-lasting neurological damage, which is attributed mainly to the excessive levels of glutamate caused by the intoxication. Glutamate toxicity, however, is not specific to OP poisoning, and is linked to propagation of damage in both acute and chronic neurodegenerativ...
journal_title：Neurotoxicity research
pub_type： 杂志文章,评审
doi：10.1007/s12640-013-9388-1
更新日期：2013-08-01 00:00:00
abstract：:Multiple system atrophy (MSA) is characterized by the formation of oligodendroglial cytoplasmic inclusions (GCIs) consisting of alpha-synuclein filaments. AlphaB-crystallin, a small chaperone protein that binds to unfolded proteins and inhibits aggregation, has been documented in GCIs. We investigated the relative abu...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/BF03033778
更新日期：2005-01-01 00:00:00
abstract：:Aging plays a significant role in the progression of vascular diseases and vascular dysfunction. Activation of the ADP-ribosylation factor 6 and small GTPases by inflammatory signals may cause vascular permeability and endothelial leakage. Pro-inflammatory molecules have a significant effect on smooth muscle cells (SM...
journal_title：Neurotoxicity research
pub_type： 杂志文章,评审
doi：10.1007/s12640-019-00047-5
更新日期：2019-10-01 00:00:00
abstract：:C57/BL6 mice were administered either 7.5 mg Fe (II)/ kg or vehicle (saline) postnatally on Days 10-12 after birth. From 64 days of age onwards for 24 days, groups of mice were administered either haloperidol (0.25 or 1 or 2 mg/kg, s.c.) or vehicle (Tween-80). Twenty-four hours after the final injection of either neur...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/BF03033321
更新日期：2006-06-01 00:00:00
abstract：:Cocaine was previously shown to act at the Sigma1R which is a target for counteracting cocaine actions. It therefore becomes of interest to test if the monoamine stabilizer (-) OSU-6162 (OSU-6162) with a nanomolar affinity for the Sigma1R can acutely modulate in low doses the effects of cocaine self-administration. In...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-019-00134-7
更新日期：2020-02-01 00:00:00
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journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/BF03033305
更新日期：2006-01-01 00:00:00
abstract：:Thioredoxin (Trx) and glyoxalase (Glo) systems have been suggested to be molecular targets of methylglyoxal (MGO). This highly reactive endogenous compound has been associated with the development of neurodegenerative pathologies and cell death. In the present study, the glutathione (GSH), Trx, and Glo systems were in...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-017-9738-5
更新日期：2017-10-01 00:00:00
abstract：:Neuronal degeneration observed in the goldfish retina after MPTP administration, displays features of apoptosis, a physiological mechanism of cell death that occurs during development. The ultrastructural features of degenerating retinal neurons, that are seen in the inner nuclear layer two days after intravitreal MPT...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/BF03033264
更新日期：2001-07-01 00:00:00
abstract：:The main pathochemical hallmark of Parkinson's disease (PD) is the loss of dopamine in the striatum of the brain, and the oral administration of levodopa (L-dopa) is a treatment that partially restores the dopaminergic transmission. In vitro assays have demonstrated both toxic and protective effects of L-dopa on dopam...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-014-9495-7
更新日期：2015-02-01 00:00:00
abstract：:Accumulating data support axonal degeneration as the major determinant of irreversible neurological disability in patients with multiple sclerosis (MS). The extent of axonal injury correlates with the degree of inflammation in active MS lesions and occurs at early stages of disease, indicating that inflammatory demyel...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/BF03033380
更新日期：2003-01-01 00:00:00
abstract：:Neural transplantation is a promising treatment strategy that can restore the motor, sensory and cognitive functions in the rat middle cerebral artery occlusion (MCAO) model of stroke. In particular, neuronal cells derived from a human teratocarcinoma cell line, called hNT neurons or LBS neurons (clinical grade prepar...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1080/10298420290015908
更新日期：2002-03-01 00:00:00
abstract：:The level of acetylcholine, a neurotransmitter essential for processing memory and learning, is lower in the brains of patients with Alzheimer's disease due to the higher concentration of the enzyme acetylcholinesterase. The main compounds used for Alzheimer's treatment are acetylcholinesterase inhibitors. Quercetin c...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-019-00142-7
更新日期：2020-04-01 00:00:00
abstract：:The process of receptor supersensitivity (RSS) has a long history and is an epiphenomenon of neuronal denervation. Dopamine (DA) RSS (DARSS) similarly occurs after DA denervation, and this process is invoked in neuropsychiatric and neurodegenerative disorders. From studies largely over the past 25 years, much has been...
journal_title：Neurotoxicity research
pub_type： 杂志文章,评审
doi：10.1007/BF03033804
更新日期：2008-10-01 00:00:00
abstract：:Parkinson's disease (PD) represents one of the neurodegenerative disorders which are caused by degeneration of dopaminergic neurons in the nigrostriatal pathway. Different toxins, e.g., 6-hydroxydopamine (6-OHDA), are used to model PD in animals. 6-OHDA is a neurotoxin which damages catecholaminergic neurons via produ...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-017-9824-8
更新日期：2018-04-01 00:00:00
abstract：:Patients scheduled for cochlear implantation often retain residual hearing in the low frequencies. Unfortunately, some patients lose their residual hearing following implantation and the reasons for this are not well understood. Evidence suggests that electrotoxicity could be one of the factors responsible for this la...
journal_title：Neurotoxicity research
pub_type： 杂志文章
doi：10.1007/s12640-019-00017-x
更新日期：2019-07-01 00:00:00
