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Change History
Changed By: apophasis
Change Date: August 27, 2010 02:24PM
[Molecular Biology] Researchers Develop Mouse Model for Study of Frontotemporal Lobar Degeneration, a Common Cause of Dementia
Change Date: August 27, 2010 02:24PM
[Molecular Biology] Researchers Develop Mouse Model for Study of Frontotemporal Lobar Degeneration, a Common Cause of Dementia
[Molecular Biology] Researchers Develop Mouse Model for Study of Frontotemporal Lobar Degeneration, a Common Cause of Dementia (<a href=http://mepopedia.com/forum/read.php?127,7457>Chinese Version</a>)
<i>Academia Sinica Newsletter</i> (2010/08/27) A team of Taiwan researchers led by Academician Che-Kun James SHEN, a Distinguished Research Fellow of the Institute of Molecular Biology, Academia Sinica, has engineered the first mouse model of Frontotemporal lobar degeneration (FTLD). The advance is expected to speed up the development of new drugs and treatments for the disease. FTLD is a common cause of dementia for which there is currently no treatment. The study was published in the <i>Journal of Experimental Medicine</i> on July 27, 2010.
FTLD is associated with atrophy in the frontal and temporal lobes of the brain, memory loss, aphasia (impairment of language ability) and sometimes motor neuron diseases. In the under 65 age group, it is the second most common cause of dementia after Alzheimers disease; and in the over 65s it is the fourth most common cause of dementia after Alzheimers disease, dementia with Lewy bodies, and vascular dementia. Recent studies have shown that dysmetabolism of a type of cellular protein, known as TAR DNA binding protein 43 (TDP-43), is closely associated with a range of neurodegenerative diseases including FTLD-U, a subclass of FTLD, and amyotrophic lateral sclerosis (ALS, a fatal neurodegenerative disease paralyzing the victim). Different gene mutations including those in the TDP-43-encoding gene are believed to contribute to these neurodegenerative disorders. Also, the level of TDP-43 protein is often found to be elevated in FTLD-U and ALS.
In this study, the researchers genetically engineered mice with increased levels of TDP-43 in the forebrain, and discovered that these mice exhibited impaired cognition and motor performances, brain atrophy and a deficit in the long-term potentiation that mimic FTLD.
The finding that increased levels of TDP-43 protein in the forebrain are sufficient to cause FTLD and possibly other neurodegenerative diseases yields a new avenue for future studies of FTLD. Using the new model Academician SHENs research team has already started to test a few potential drugs for treating FTLD. A collaboration with a laboratory based in Australia has also been established for drug screening.
Related Website: http://jem.rupress.org/content/207/8/1661.abstract
Media Contacts:
Dr. Che-Kun James SHEN, Institute of Molecular Biology, Academia Sinica
(Tel) +886-2-2782-4188
ckshen@imb.sinica.edu.tw
Fang-Hsun YEH, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8820, (Fax) +886-2-2782-1551, (M)0922-036-691
hongsum@gate.sinica.edu.tw
Mei-Hui LIN, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8821, (Fax) +886-2-2782-1551, (M) 0921-845-234
mhlin313@gate.sinica.edu.tw
Reference:
<a href=http://www.sinica.edu.tw/manage/gatenews/showsingle.php?_op=?rid:3463%26isEnglish:1>Academia Sinica Newsletter 2010/08/27</a>
<i>Academia Sinica Newsletter</i> (2010/08/27) A team of Taiwan researchers led by Academician Che-Kun James SHEN, a Distinguished Research Fellow of the Institute of Molecular Biology, Academia Sinica, has engineered the first mouse model of Frontotemporal lobar degeneration (FTLD). The advance is expected to speed up the development of new drugs and treatments for the disease. FTLD is a common cause of dementia for which there is currently no treatment. The study was published in the <i>Journal of Experimental Medicine</i> on July 27, 2010.
FTLD is associated with atrophy in the frontal and temporal lobes of the brain, memory loss, aphasia (impairment of language ability) and sometimes motor neuron diseases. In the under 65 age group, it is the second most common cause of dementia after Alzheimers disease; and in the over 65s it is the fourth most common cause of dementia after Alzheimers disease, dementia with Lewy bodies, and vascular dementia. Recent studies have shown that dysmetabolism of a type of cellular protein, known as TAR DNA binding protein 43 (TDP-43), is closely associated with a range of neurodegenerative diseases including FTLD-U, a subclass of FTLD, and amyotrophic lateral sclerosis (ALS, a fatal neurodegenerative disease paralyzing the victim). Different gene mutations including those in the TDP-43-encoding gene are believed to contribute to these neurodegenerative disorders. Also, the level of TDP-43 protein is often found to be elevated in FTLD-U and ALS.
In this study, the researchers genetically engineered mice with increased levels of TDP-43 in the forebrain, and discovered that these mice exhibited impaired cognition and motor performances, brain atrophy and a deficit in the long-term potentiation that mimic FTLD.
The finding that increased levels of TDP-43 protein in the forebrain are sufficient to cause FTLD and possibly other neurodegenerative diseases yields a new avenue for future studies of FTLD. Using the new model Academician SHENs research team has already started to test a few potential drugs for treating FTLD. A collaboration with a laboratory based in Australia has also been established for drug screening.
Related Website: http://jem.rupress.org/content/207/8/1661.abstract
Media Contacts:
Dr. Che-Kun James SHEN, Institute of Molecular Biology, Academia Sinica
(Tel) +886-2-2782-4188
ckshen@imb.sinica.edu.tw
Fang-Hsun YEH, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8820, (Fax) +886-2-2782-1551, (M)0922-036-691
hongsum@gate.sinica.edu.tw
Mei-Hui LIN, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8821, (Fax) +886-2-2782-1551, (M) 0921-845-234
mhlin313@gate.sinica.edu.tw
Reference:
<a href=http://www.sinica.edu.tw/manage/gatenews/showsingle.php?_op=?rid:3463%26isEnglish:1>Academia Sinica Newsletter 2010/08/27</a>
Changed By: apophasis
Change Date: August 27, 2010 02:20PM
[Medicine] [Molecular Biology] Researchers Develop Mouse Model for Study of Frontotemporal Lobar Degeneration, a Common Cause of Dementia
Change Date: August 27, 2010 02:20PM
[Medicine] [Molecular Biology] Researchers Develop Mouse Model for Study of Frontotemporal Lobar Degeneration, a Common Cause of Dementia
[Medicine] [Molecular Biology] Researchers Develop Mouse Model for Study of Frontotemporal Lobar Degeneration, a Common Cause of Dementia (<a href=>Chinese Version</a>)
<i>Academia Sinica Newsletter</i> (2010/08/27) A team of Taiwan researchers led by Academician Che-Kun James SHEN, a Distinguished Research Fellow of the Institute of Molecular Biology, Academia Sinica, has engineered the first mouse model of Frontotemporal lobar degeneration (FTLD). The advance is expected to speed up the development of new drugs and treatments for the disease. FTLD is a common cause of dementia for which there is currently no treatment. The study was published in the <i>Journal of Experimental Medicine</i> on July 27, 2010.
FTLD is associated with atrophy in the frontal and temporal lobes of the brain, memory loss, aphasia (impairment of language ability) and sometimes motor neuron diseases. In the under 65 age group, it is the second most common cause of dementia after Alzheimers disease; and in the over 65s it is the fourth most common cause of dementia after Alzheimers disease, dementia with Lewy bodies, and vascular dementia. Recent studies have shown that dysmetabolism of a type of cellular protein, known as TAR DNA binding protein 43 (TDP-43), is closely associated with a range of neurodegenerative diseases including FTLD-U, a subclass of FTLD, and amyotrophic lateral sclerosis (ALS, a fatal neurodegenerative disease paralyzing the victim). Different gene mutations including those in the TDP-43-encoding gene are believed to contribute to these neurodegenerative disorders. Also, the level of TDP-43 protein is often found to be elevated in FTLD-U and ALS.
In this study, the researchers genetically engineered mice with increased levels of TDP-43 in the forebrain, and discovered that these mice exhibited impaired cognition and motor performances, brain atrophy and a deficit in the long-term potentiation that mimic FTLD.
The finding that increased levels of TDP-43 protein in the forebrain are sufficient to cause FTLD and possibly other neurodegenerative diseases yields a new avenue for future studies of FTLD. Using the new model Academician SHENs research team has already started to test a few potential drugs for treating FTLD. A collaboration with a laboratory based in Australia has also been established for drug screening.
Related Website: http://jem.rupress.org/content/207/8/1661.abstract
Media Contacts:
Dr. Che-Kun James SHEN, Institute of Molecular Biology, Academia Sinica
(Tel) +886-2-2782-4188
ckshen@imb.sinica.edu.tw
Fang-Hsun YEH, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8820, (Fax) +886-2-2782-1551, (M)0922-036-691
hongsum@gate.sinica.edu.tw
Mei-Hui LIN, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8821, (Fax) +886-2-2782-1551, (M) 0921-845-234
mhlin313@gate.sinica.edu.tw
Reference:
<a href=http://www.sinica.edu.tw/manage/gatenews/showsingle.php?_op=?rid:3463%26isEnglish:1>Academia Sinica Newsletter 2010/08/27</a>
<i>Academia Sinica Newsletter</i> (2010/08/27) A team of Taiwan researchers led by Academician Che-Kun James SHEN, a Distinguished Research Fellow of the Institute of Molecular Biology, Academia Sinica, has engineered the first mouse model of Frontotemporal lobar degeneration (FTLD). The advance is expected to speed up the development of new drugs and treatments for the disease. FTLD is a common cause of dementia for which there is currently no treatment. The study was published in the <i>Journal of Experimental Medicine</i> on July 27, 2010.
FTLD is associated with atrophy in the frontal and temporal lobes of the brain, memory loss, aphasia (impairment of language ability) and sometimes motor neuron diseases. In the under 65 age group, it is the second most common cause of dementia after Alzheimers disease; and in the over 65s it is the fourth most common cause of dementia after Alzheimers disease, dementia with Lewy bodies, and vascular dementia. Recent studies have shown that dysmetabolism of a type of cellular protein, known as TAR DNA binding protein 43 (TDP-43), is closely associated with a range of neurodegenerative diseases including FTLD-U, a subclass of FTLD, and amyotrophic lateral sclerosis (ALS, a fatal neurodegenerative disease paralyzing the victim). Different gene mutations including those in the TDP-43-encoding gene are believed to contribute to these neurodegenerative disorders. Also, the level of TDP-43 protein is often found to be elevated in FTLD-U and ALS.
In this study, the researchers genetically engineered mice with increased levels of TDP-43 in the forebrain, and discovered that these mice exhibited impaired cognition and motor performances, brain atrophy and a deficit in the long-term potentiation that mimic FTLD.
The finding that increased levels of TDP-43 protein in the forebrain are sufficient to cause FTLD and possibly other neurodegenerative diseases yields a new avenue for future studies of FTLD. Using the new model Academician SHENs research team has already started to test a few potential drugs for treating FTLD. A collaboration with a laboratory based in Australia has also been established for drug screening.
Related Website: http://jem.rupress.org/content/207/8/1661.abstract
Media Contacts:
Dr. Che-Kun James SHEN, Institute of Molecular Biology, Academia Sinica
(Tel) +886-2-2782-4188
ckshen@imb.sinica.edu.tw
Fang-Hsun YEH, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8820, (Fax) +886-2-2782-1551, (M)0922-036-691
hongsum@gate.sinica.edu.tw
Mei-Hui LIN, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8821, (Fax) +886-2-2782-1551, (M) 0921-845-234
mhlin313@gate.sinica.edu.tw
Reference:
<a href=http://www.sinica.edu.tw/manage/gatenews/showsingle.php?_op=?rid:3463%26isEnglish:1>Academia Sinica Newsletter 2010/08/27</a>
Original Message
雿: apophasisDate: August 27, 2010 02:19PM
[Medicine] Researchers Develop Mouse Model for Study of Frontotemporal Lobar Degeneration, a Common Cause of Dementia
[Medicine] Researchers Develop Mouse Model for Study of Frontotemporal Lobar Degeneration, a Common Cause of Dementia (Chinese Version)
Academia Sinica Newsletter (2010/08/27) A team of Taiwan researchers led by Academician Che-Kun James SHEN, a Distinguished Research Fellow of the Institute of Molecular Biology, Academia Sinica, has engineered the first mouse model of Frontotemporal lobar degeneration (FTLD). The advance is expected to speed up the development of new drugs and treatments for the disease. FTLD is a common cause of dementia for which there is currently no treatment. The study was published in the Journal of Experimental Medicine on July 27, 2010.
FTLD is associated with atrophy in the frontal and temporal lobes of the brain, memory loss, aphasia (impairment of language ability) and sometimes motor neuron diseases. In the under 65 age group, it is the second most common cause of dementia after Alzheimers disease; and in the over 65s it is the fourth most common cause of dementia after Alzheimers disease, dementia with Lewy bodies, and vascular dementia. Recent studies have shown that dysmetabolism of a type of cellular protein, known as TAR DNA binding protein 43 (TDP-43), is closely associated with a range of neurodegenerative diseases including FTLD-U, a subclass of FTLD, and amyotrophic lateral sclerosis (ALS, a fatal neurodegenerative disease paralyzing the victim). Different gene mutations including those in the TDP-43-encoding gene are believed to contribute to these neurodegenerative disorders. Also, the level of TDP-43 protein is often found to be elevated in FTLD-U and ALS.
In this study, the researchers genetically engineered mice with increased levels of TDP-43 in the forebrain, and discovered that these mice exhibited impaired cognition and motor performances, brain atrophy and a deficit in the long-term potentiation that mimic FTLD.
The finding that increased levels of TDP-43 protein in the forebrain are sufficient to cause FTLD and possibly other neurodegenerative diseases yields a new avenue for future studies of FTLD. Using the new model Academician SHENs research team has already started to test a few potential drugs for treating FTLD. A collaboration with a laboratory based in Australia has also been established for drug screening.
Related Website: http://jem.rupress.org/content/207/8/1661.abstract
Media Contacts:
Dr. Che-Kun James SHEN, Institute of Molecular Biology, Academia Sinica
(Tel) +886-2-2782-4188
ckshen@imb.sinica.edu.tw
Fang-Hsun YEH, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8820, (Fax) +886-2-2782-1551, (M)0922-036-691
hongsum@gate.sinica.edu.tw
Mei-Hui LIN, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8821, (Fax) +886-2-2782-1551, (M) 0921-845-234
mhlin313@gate.sinica.edu.tw
Reference:
Academia Sinica Newsletter 2010/08/27
Academia Sinica Newsletter (2010/08/27) A team of Taiwan researchers led by Academician Che-Kun James SHEN, a Distinguished Research Fellow of the Institute of Molecular Biology, Academia Sinica, has engineered the first mouse model of Frontotemporal lobar degeneration (FTLD). The advance is expected to speed up the development of new drugs and treatments for the disease. FTLD is a common cause of dementia for which there is currently no treatment. The study was published in the Journal of Experimental Medicine on July 27, 2010.
FTLD is associated with atrophy in the frontal and temporal lobes of the brain, memory loss, aphasia (impairment of language ability) and sometimes motor neuron diseases. In the under 65 age group, it is the second most common cause of dementia after Alzheimers disease; and in the over 65s it is the fourth most common cause of dementia after Alzheimers disease, dementia with Lewy bodies, and vascular dementia. Recent studies have shown that dysmetabolism of a type of cellular protein, known as TAR DNA binding protein 43 (TDP-43), is closely associated with a range of neurodegenerative diseases including FTLD-U, a subclass of FTLD, and amyotrophic lateral sclerosis (ALS, a fatal neurodegenerative disease paralyzing the victim). Different gene mutations including those in the TDP-43-encoding gene are believed to contribute to these neurodegenerative disorders. Also, the level of TDP-43 protein is often found to be elevated in FTLD-U and ALS.
In this study, the researchers genetically engineered mice with increased levels of TDP-43 in the forebrain, and discovered that these mice exhibited impaired cognition and motor performances, brain atrophy and a deficit in the long-term potentiation that mimic FTLD.
The finding that increased levels of TDP-43 protein in the forebrain are sufficient to cause FTLD and possibly other neurodegenerative diseases yields a new avenue for future studies of FTLD. Using the new model Academician SHENs research team has already started to test a few potential drugs for treating FTLD. A collaboration with a laboratory based in Australia has also been established for drug screening.
Related Website: http://jem.rupress.org/content/207/8/1661.abstract
Media Contacts:
Dr. Che-Kun James SHEN, Institute of Molecular Biology, Academia Sinica
(Tel) +886-2-2782-4188
ckshen@imb.sinica.edu.tw
Fang-Hsun YEH, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8820, (Fax) +886-2-2782-1551, (M)0922-036-691
hongsum@gate.sinica.edu.tw
Mei-Hui LIN, Public Affairs Office, Central Office of Administration, Academia Sinica
(Tel) +886-2-2789-8821, (Fax) +886-2-2782-1551, (M) 0921-845-234
mhlin313@gate.sinica.edu.tw
Reference:
Academia Sinica Newsletter 2010/08/27
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