Neuronal Vacuolation in the Basal Nucleus of Meynert Caused by Fetal Hydrocephalus

2002 ◽  
Vol 36 (6) ◽  
pp. 320-323 ◽  
Author(s):  
Norbert Ulfig
Keyword(s):  
Basal Nucleus ◽  
Fetal Hydrocephalus ◽  
Basal Nucleus Of Meynert ◽  
Neuronal Vacuolation

scholarly journals Tau and TDP-43 accumulation of the basal nucleus of Meynert in individuals with cerebral lobar infarcts or hemorrhage

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Hiroyuki Hatsuta ◽  
Masaki Takao ◽  
Akane Nogami ◽  
Akiko Uchino ◽  
Hiroyuki Sumikura ◽  
...  
Keyword(s):  
Basal Nucleus ◽  
Basal Nucleus Of Meynert

Basal nucleus of meynert

1983 ◽  
Vol 62 (1-3) ◽  
pp. 243-260 ◽  
Author(s):  
F. Tagliavini ◽  
G. Pilleri
Keyword(s):  
Basal Nucleus ◽  
Basal Nucleus Of Meynert

Autoradiographic demonstration of 5HT1 binding sites in the primate basal nucleus of Meynert

1984 ◽  
Vol 104 (1-2) ◽  
pp. 189-190 ◽  
Author(s):  
I.J. Mitchell ◽  
A.M. Stuart ◽  
P. Slater ◽  
H.P. Unwin ◽  
A.R. Crossman
Keyword(s):  
Binding Sites ◽  
Basal Nucleus ◽  
Basal Nucleus Of Meynert

scholarly journals S100b Counteracts Neurodegeneration of Rat Cholinergic Neurons in Brain Slices after Oxygen-Glucose Deprivation

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Daniela Serbinek ◽  
Celine Ullrich ◽  
Michael Pirchl ◽  
Tanja Hochstrasser ◽  
Rainald Schmidt-Kastner ◽  
...  
Keyword(s):  
Growth Factor ◽  
Neurodegenerative Disorder ◽  
Brain Slices ◽  
Metabolic Stress ◽  
Cholinergic Neurons ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Basal Nucleus ◽  
Ischemic Events ◽  
Basal Nucleus Of Meynert

Alzheimer's disease is a severe chronic neurodegenerative disorder characterized by beta-amyloid plaques, tau pathology, cerebrovascular damage, inflammation, reactive gliosis, and cell death of cholinergic neurons. The aim of the present study is to test whether the glia-derived molecule S100b can counteract neurodegeneration of cholinergic neurons after oxygen-glucose deprivation (OGD) in organotypic brain slices of basal nucleus of Meynert. Our data showed that 3 days of OGD induced a marked decrease of cholinergic neurons (60% of control), which could be counteracted by 50 μg/mL recombinant S100b. The effect was dose and time dependent. Application of nerve growth factor or fibroblast growth factor-2 was less protective. C-fos-like immunoreactivity was enhanced 3 hours after OGD indicating metabolic stress. We conclude that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.

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