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Alzheimer's, Dementia & Mental Health
New Tool May Lead to Treating Earliest Stage of
Alzheimer's and Halting Progression
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Alois Alzheimer
Read bio below news story. |
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Yeast model revealed 100 years after Alois
Alzheimer discovered the disease
November 19, 2006 - A century ago this month, German psychiatrist Alois
Alzheimer formally described characteristics of the neurodegenerative
disease, which he called "presenile dementia." It ultimately came to
bear his name. While international efforts to learn about Alzheimer's
disease and develop treatments have progressed significantly in recent
years, a cure remains an elusive goal. But a new tool may lead to
stopping the progress of AD, when diagnosed early.
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Alzheimer's, Dementia & Mental Health |
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Alzheimer's disease is characterized by the
formation of plaques in the brain largely composed of fibers made from a
peptide called beta-amyloid, or A-beta, for short.
There is abundant evidence to support the
hypothesis that accumulation of A-beta peptide triggers the appearance
of Alzheimer's. But while earlier research suggested the A-beta fiber
caused Alzheimer's, recent research points at much smaller aggregates of
the peptide as the culprit.
This new research tool was developed by Susan
Liebman, distinguished university professor of biological sciences at
the University of Illinois at Chicago.
"We've developed a yeast model system in which
A-beta small aggregate formation can be detected," said Liebman.
"The
system employs a fusion of the human A-beta peptide to a functional
yeast protein, called a reporter protein, which is only active in
allowing cells to grow on test media if the fusion does not form
aggregates."
Liebman said the yeast model system can be used to
develop a high throughput assay to screen small molecules to find those
that inhibit the A-beta dependent aggregation. "We'll screen a library
of drugs and compounds, looking for ones that allow our yeast with the
reporter protein to grow."
She said after the assay conditions are perfected,
the screen will be ready for an automated process that will allow for
fast testing of many compounds. Medicinal chemists would then study the
structures of compounds that pass the screen and design compounds that
enhance the activity without being toxic. Animal and human trials would
follow.
"One promising, emerging approach for treatment of
Alzheimer's disease is to prevent these smaller aggregates from
forming," said Liebman.
"Disruption of these small aggregates rather than
the larger fibers seems prudent since inhibition of A-beta fiber
formation might cause the smaller aggregate species to accumulate, and
since inhibiting smaller aggregate formation should also prevent the
initial formation of the fibers."
Some surmised this idea may ultimately provide a
means for treating the earliest stage of Alzheimer's, thereby stemming
its progression.
Editor's Notes:
The findings were reported in BMC Biology. It was
the journal's most viewed article this past month. UIC graduate student
Sviatoslav Bagriantsev worked on the project in Liebman's laboratory and
co-authored the paper.
Alois Alzheimer
From Wikipedia, the free encyclopedia
Aloysius "Alois" Alzheimer (b. June 14, 1864 in
Marktbreit, Bavaria; d. December 19, 1915 in Breslau, now Wrocław,
Poland) was a German psychiatrist and neuropathologist and a colleague
of Emil Kraepelin. Alzheimer is credited with the first published case
of 'presenile dementia', which Kraepelin would later identify as
Alzheimer's disease.
Alzheimer's father served in the office of notary
public in the family's hometown. Alzheimer attended Aschaffenburg,
Tόbingen, Berlin, and Wόrzburg universities. He received a medical
degree at Wόrzburg University in 1887. In the following year, he spent
five months assisting mentally ill women, before he took an office in
the city mental asylum in Frankfurt am Main: the Stδdtische Anstalt fόr
Irre und Epileptische (asylum for lunatics and epileptics). Emil Sioli
was the dean of that asylum (1852-1922). Another neurologist, Franz
Nissl (1860-1919), began to work in that same asylum with Alzheimer, and
they knew each other.
Much of Alzheimer's later work on brain pathology
made use of Nissl's method of silver staining of the histological
sections. Alzheimer was the co-founder and co-publisher of the journal
Zeitschrift fόr die gesamte Neurologie und Psychiatrie. He never wrote a
book that he could call his own.
In 1901, Alzheimer observed a patient at the
Frankfurt Asylum named Mrs. Auguste Deter. The 51 year-old patient had
strange behavioral include a loss of short term memory. This patient
would become his obsession over the coming years. In April, 1906, Mrs.
Deter died and Alzheimer had the patient records and the brain sent to
Munich where he was working at Kraepelin's lab. Together with two
Italian physicians, he would use the staining techniques to identify
amyloid plaques and neurofibrilary tangles. A speech given on November
3, 1906 would be the first time the pathology and the clinical symptoms
of presenile dementia would be presented together.
Since German was the common language of science
and especially of Psychology of the time, Kraepelin's use of Alzheimer's
disease in a text book would make the name famous. By 1911, the disease
was being used by European physicians to diagnose patients in the US.
[1]
Alzheimer fell ill on the train on the way to the
University of Breslau where he had been appointed professor of
psychiatry in 1912. Most probably he had a streptococcal infection and
subsequent rheumatic fever and kidney failure. He died of heart failure
at the age of 51 in Breslau.
>>>
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