Selective vulnerability in the gerbil hippocampus following transient ischemia

1984 ◽  
Vol 62 (3) ◽  
pp. 201-208 ◽  
Author(s):  
T. Kirino ◽  
K. Sano
Keyword(s):  
Selective Vulnerability ◽  
Transient Ischemia

[14C]Leucine Incorporation into Brain Proteins in Gerbils After Transient Ischemia: Relationship to Selective Vulnerability of Hippocampus

1991 ◽  
Vol 56 (3) ◽  
pp. 789-796 ◽  
Author(s):  
R. Widmann ◽  
T. Kuroiwa ◽  
P. Bonnekoh ◽  
K.-A. Hossmann
Keyword(s):  
Selective Vulnerability ◽  
Leucine Incorporation ◽  
Transient Ischemia ◽  
Brain Proteins

Immunohistochemical localization of lysosomal cysteine protease cathepsins B and L in monkey hippocampal neurons after transient ischemia

1999 ◽  
Vol 19 (3) ◽  
pp. 302-310
Author(s):  
Yukihiko Kohda ◽  
Katsuhiro Tsuchiya ◽  
Junkoh Yamashita ◽  
Masaki Yoshida ◽  
Takashi Ueno ◽  
...  
Keyword(s):  
Cysteine Protease ◽  
Hippocampal Neurons ◽  
Immunohistochemical Localization ◽  
Transient Ischemia ◽  
Lysosomal Cysteine Protease

Effects of isoflurane on the ischemia-induced release of excitatory amino acids, brain swelling and injury in a model of transient ischemia in rats

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S439-S439
Author(s):  
Marie-Françoise Ritz ◽  
Petra Schmidt ◽  
Aminadav Mendelowitsch
Keyword(s):  
Amino Acids ◽  
Excitatory Amino Acids ◽  
Brain Swelling ◽  
Transient Ischemia

In a rat model of transient ischemia, acute albumin leakage across the blood-brain barrier is often followed by rapid cellular uptake

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S277-S277
Author(s):  
Tavarekere N Nagaraja ◽  
Kelly A Keenan ◽  
Joseph D Fenstermacher ◽  
Robert A Knight
Keyword(s):  
Blood Brain Barrier ◽  
Cellular Uptake ◽  
Rat Model ◽  
Brain Barrier ◽  
Transient Ischemia ◽  
Blood Brain ◽  
Albumin Leakage

scholarly journals Integrating the Roles of Midbrain Dopamine Circuits in Behavior and Neuropsychiatric Disease

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 647
Author(s):  
Allen PF Chen ◽  
Lu Chen ◽  
Thomas A. Kim ◽  
Qiaojie Xiong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neural Circuit ◽  
Selective Vulnerability ◽  
Dependent Manner ◽  
Memory Processing ◽  
Systems Neuroscience ◽  
Neuropsychiatric Diseases ◽  
Midbrain Dopamine ◽  
Dopamine Circuits

Dopamine (DA) is a behaviorally and clinically diverse neuromodulator that controls CNS function. DA plays major roles in many behaviors including locomotion, learning, habit formation, perception, and memory processing. Reflecting this, DA dysregulation produces a wide variety of cognitive symptoms seen in neuropsychiatric diseases such as Parkinson’s, Schizophrenia, addiction, and Alzheimer’s disease. Here, we review recent advances in the DA systems neuroscience field and explore the advancing hypothesis that DA’s behavioral function is linked to disease deficits in a neural circuit-dependent manner. We survey different brain areas including the basal ganglia’s dorsomedial/dorsolateral striatum, the ventral striatum, the auditory striatum, and the hippocampus in rodent models. Each of these regions have different reported functions and, correspondingly, DA’s reflecting role in each of these regions also has support for being different. We then focus on DA dysregulation states in Parkinson’s disease, addiction, and Alzheimer’s Disease, emphasizing how these afflictions are linked to different DA pathways. We draw upon ideas such as selective vulnerability and region-dependent physiology. These bodies of work suggest that different channels of DA may be dysregulated in different sets of disease. While these are great advances, the fine and definitive segregation of such pathways in behavior and disease remains to be seen. Future studies will be required to define DA’s necessity and contribution to the functional plasticity of different striatal regions.

scholarly journals Cortical Excitability across the ALS Clinical Motor Phenotypes

2021 ◽  
Vol 11 (6) ◽  
pp. 715
Author(s):  
Thanuja Dharmadasa
Keyword(s):  
Motor Cortex ◽  
Cortical Excitability ◽  
Phenotypic Variability ◽  
Specific Treatment ◽  
Underlying Disease ◽  
Selective Vulnerability ◽  
Clinical Feature ◽  
Cortical Hyperexcitability ◽  
Wide Range

Amyotrophic lateral sclerosis (ALS) is characterized by its marked clinical heterogeneity. Although the coexistence of upper and lower motor neuron signs is a common clinical feature for most patients, there is a wide range of atypical motor presentations and clinical trajectories, implying a heterogeneity of underlying pathogenic mechanisms. Corticomotoneuronal dysfunction is increasingly postulated as the harbinger of clinical disease, and neurophysiological exploration of the motor cortex in vivo using transcranial magnetic stimulation (TMS) has suggested that motor cortical hyperexcitability may be a critical pathogenic factor linked to clinical features and survival. Region-specific selective vulnerability at the level of the motor cortex may drive the observed differences of clinical presentation across the ALS motor phenotypes, and thus, further understanding of phenotypic variability in relation to cortical dysfunction may serve as an important guide to underlying disease mechanisms. This review article analyses the cortical excitability profiles across the clinical motor phenotypes, as assessed using TMS, and explores this relationship to clinical patterns and survival. This understanding will remain essential to unravelling central disease pathophysiology and for the development of specific treatment targets across the ALS clinical motor phenotypes.

Selective vulnerability of alpha motor neurons in ALS: Relation to autoantibodies toward acetylcholinesterase (AChE) in ALS patients

1993 ◽  
Vol 30 (3-4) ◽  
pp. 369-371 ◽  
Author(s):  
Sebastian Conradi ◽  
Lars-Olof Ronnevi
Keyword(s):  
Motor Neurons ◽  
Selective Vulnerability ◽  
Als Patients

scholarly journals Transcriptional perturbation of protein arginine methyltransferase-5 exhibits MTAP-selective oncosuppression

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sara Busacca ◽  
Qi Zhang ◽  
Annabel Sharkey ◽  
Alan G. Dawson ◽  
David A. Moore ◽  
...  
Keyword(s):  
Small Molecule ◽  
Selective Vulnerability ◽  
Dependent Manner ◽  
Histone H4 ◽  
Wild Type ◽  
Protein Arginine Methyltransferase ◽  
Arginine Methyltransferase ◽  
Methylthioadenosine Phosphorylase ◽  
Protein Arginine Methyltransferase 5

AbstractWe hypothesized that small molecule transcriptional perturbation could be harnessed to target a cellular dependency involving protein arginine methyltransferase 5 (PRMT5) in the context of methylthioadenosine phosphorylase (MTAP) deletion, seen frequently in malignant pleural mesothelioma (MPM). Here we show, that MTAP deletion is negatively prognostic in MPM. In vitro, the off-patent antibiotic Quinacrine efficiently suppressed PRMT5 transcription, causing chromatin remodelling with reduced global histone H4 symmetrical demethylation. Quinacrine phenocopied PRMT5 RNA interference and small molecule PRMT5 inhibition, reducing clonogenicity in an MTAP-dependent manner. This activity required a functional PRMT5 methyltransferase as MTAP negative cells were rescued by exogenous wild type PRMT5, but not a PRMT5E444Q methyltransferase-dead mutant. We identified c-jun as an essential PRMT5 transcription factor and a probable target for Quinacrine. Our results therefore suggest that small molecule-based transcriptional perturbation of PRMT5 can leverage a mutation-selective vulnerability, that is therapeutically tractable, and has relevance to 9p21 deleted cancers including MPM.

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