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Modulation of protein accumulation and uses therefor

A protein and protein technology, applied in the regulation of protein accumulation and its application field, can solve the problem of indistinguishable ALS cases

Pending Publication Date: 2019-08-30
MACQUARIE UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

[0006] About 10% of ALS cases have a positive family history (familial ALS) and are clinically indistinguishable from sporadic ALS cases

Method used

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  • Modulation of protein accumulation and uses therefor
  • Modulation of protein accumulation and uses therefor
  • Modulation of protein accumulation and uses therefor

Examples

Experimental program
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Effect test

Embodiment 1

[0275] Expression of a wild-type CCNF transgene reduces pathological levels of TDP-43 in neurons expressing mutant TDP-43 alleles associated with ALS

[0276] TDP-43 A315T Mice express human TDP-43 carrying the pathogenic A315T ALS mutation under the control of a neuron-inducible promoter system (Ke et al., 2015, supra). In the absence of doxycycline (Dox), TDP-43 A315T Mice express the transgene in neurons of the CNS, including the motor cortex and spinal cord. TDP-43 A315T Mice develop early-onset and progressive motor deficits and muscle atrophy. in biochemistry, the TDP-43 A315T Accumulation of insoluble cytoplasmic TDP-43 was found in mice, along with significant neuronal loss.

[0277] To investigate whether wild-type CCNF expression could rescue the accumulation of insoluble cytoplasmic TDP-43, AAV9-CCNF (1x10 12 virus particles) injected into nascent TDP-43 A315T transgenic mice and removed Dox from their food at 4 weeks of age to induce TDP-43 A315T Express. ...

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Abstract

Disclosed are compositions and methods for inhibiting abnormal protein accumulation, promoting motor neuron survival, inhibiting motor neuron degeneration and treating neurodegenerative conditions through expression of a nucleic acid sequence encoding cyclin F in motor neurons with an abnormally low level or activity of cyclin F. Also disclosed are methods for identifying agents that promote survival of motor neurons, inhibit degeneration of motor neurons and / or inhibit abnormal protein accumulation in motor neurons, identifying agents that are useful for treating neurodegenerative conditions,diagnosing neurodegenerative conditions, predicting the progression of neurodegenerative conditions, and monitoring the effectiveness of a therapy in reducing the progression of a neurodegenerative condition.

Description

[0001] field of invention [0002] This application claims Australian Provisional Application No. 2016904541, filed 7 November 2016, entitled "Modulation of protein accumulation and uses therefor" and Australian Provisional Application No. 2016904541, filed 23 March 2017, entitled "Modulation of protein accumulation and uses therefor" Priority to Australian Provisional Patent Application No. 2017901026, the contents of which are hereby incorporated by reference in their entirety. [0003] The present invention relates generally to neurodegenerative conditions. More specifically, the present invention relates to a method for inhibiting abnormal protein accumulation, promoting motor neuron survival, inhibiting motor neuron degeneration by expressing a nucleic acid sequence encoding cyclin F in motor neurons having abnormally low levels or activity of cyclin F and compositions and methods for treating neurodegenerative conditions. The present invention also relates to methods for...

Claims

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Application Information

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Patent Type & Authority Applications(China)
IPC IPC(8): C12N15/861C12Q1/6883A61K48/00A61P25/28
CPCA61K48/00C12Q1/6883C12Q2600/158C12N15/86C12N2750/14141A61P25/02A61P25/28A61K48/0058C07K14/4738C12N2750/14143G01N33/5023G01N33/5058G01N2500/10G01N2800/2814G01N2800/52G01N2800/56C12N15/861
Inventor 斯蒂芬妮·瑞纳艾伯特·李罗杰·钟伊恩·布莱尔
Owner MACQUARIE UNIV
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