Reverse genetics of the mouse central nervous system: Targeted genetic analysis of neuropeptide function and reverse genetic screens for genes involved in human neurodegenerative disease

1994 ◽  
Vol 42 (2) ◽  
pp. 319-331 ◽  
Author(s):  
R.Wayne Davies ◽  
Ed J. gallagher ◽  
Armand Savioz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Genetic Analysis ◽  
Neurodegenerative Disease ◽  
Reverse Genetics ◽  
Reverse Genetic ◽  
Genetic Screens ◽  
Human Neurodegenerative Disease ◽  
Mouse Central Nervous System

scholarly journals CB1 and LPA1 Receptors Relationship in the Mouse Central Nervous System

2019 ◽  
Vol 12 ◽  
Author(s):  
Estíbaliz González de San Román ◽  
Iván Manuel ◽  
Catherine Ledent ◽  
Jerold Chun ◽  
Fernando Rodríguez de Fonseca ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mouse Central Nervous System

scholarly journals Apoptotic Cells, Including Macrophages, Are Prominent in Theiler's Virus-Induced Inflammatory, Demyelinating Lesions

2003 ◽  
Vol 77 (7) ◽  
pp. 4383-4388 ◽  
Author(s):  
Brian P. Schlitt ◽  
Matthew Felrice ◽  
Mary Lou Jelachich ◽  
Howard L. Lipton
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
In Situ Hybridization ◽  
Apoptotic Cells ◽  
Theiler's Virus ◽  
Demyelinating Lesions ◽  
Encephalomyelitis Virus ◽  
Mouse Central Nervous System

ABSTRACT Theiler's murine encephalomyelitis virus (TMEV) persists in the mouse central nervous system principally in macrophages, and infected macrophages in culture undergo apoptosis. We have detected abundant apoptotic cells in perivascular cuffs and inflammatory, demyelinating lesions of SJL mice chronically infected with TMEV. T cells comprised 74% of apoptotic cells, while 8% were macrophages, 0.6% were astrocytes, and ∼17% remained unidentified. In situ hybridization revealed viral RNA in ∼1% of apoptotic cells.

scholarly journals Targeted DNA transfection into the mouse central nervous system using laser-induced stress waves

2005 ◽  
Vol 10 (6) ◽  
pp. 060501 ◽  
Author(s):  
Yasushi Satoh ◽  
Yasunari Kanda ◽  
Mitsuhiro Terakawa ◽  
Minoru Obara ◽  
Katsushige Mizuno ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Stress Waves ◽  
Dna Transfection ◽  
Induced Stress ◽  
Mouse Central Nervous System

scholarly journals Elevated expression of membrane type 1 metalloproteinase (MT1-MMP) in reactive astrocytes following neurodegeneration in mouse central nervous system

FEBS Letters ◽  
2000 ◽  
Vol 481 (3) ◽  
pp. 227-234 ◽  
Author(s):  
Silvia Rathke-Hartlieb ◽  
Petra Budde ◽  
Stefan Ewert ◽  
Uwe Schlomann ◽  
Martin Sebastian Staege ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Reactive Astrocytes ◽  
Elevated Expression ◽  
Membrane Type ◽  
Mouse Central Nervous System

scholarly journals Floor plate descendants in the ependyma of the adult mouse Central Nervous System

2017 ◽  
Vol 61 (3-4-5) ◽  
pp. 257-265 ◽  
Author(s):  
Sophie Khazanov ◽  
Yael Paz ◽  
Amit Hefetz ◽  
Ben J. Gonzales ◽  
Yaara Netser ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adult Mouse ◽  
Floor Plate ◽  
Mouse Central Nervous System

scholarly journals Dying to Fall Asleep

2019 ◽  
pp. 724-742
Author(s):  
Jessica Vensel Rundo ◽  
Hillor Mehta ◽  
Reena Mehra
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Genetic Analysis ◽  
Genetic Disease ◽  
Prion Proteins ◽  
Amyloid Plaques ◽  
Definitive Diagnosis ◽  
Common Features ◽  
The Central Nervous System ◽  
Autonomic Hyperactivity

Fatal familial insomnia (FFI) is a rare autosomal dominant genetic disease characterized by progressive insomnia, autonomic hyperactivity, memory deficits, hallucinations, and myoclonus. Unlike its name, insomnia is not the most common initial presentation in patients with FFI. More common features like autonomic hyperactivity (hypertension and tachycardia) are often missed, delaying the diagnosis of FFI. Genetic analysis of FFI shows a D178N-129M mutation that results in generation of insoluble proteins (prion proteins) that aggregate to form amyloid plaques, leading to deterioration of the central nervous system, particularly in the hypothalamus. This case illustrates the difficulty in determining a definitive diagnosis in patients with FFI. Unfortunately, no treatment or cure is available for FFI. The disease is fatal in all the patients.

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