studi menunjukkan , Gangguan bipolar memiliki link genetik untuk autisme
Temuan dari dua pendekatan menambah bukti
kerentanan genetik dibagi di gangguan kejiwaan utama
Date:
May 4, 2016
Source:
University of Iowa
Health Care
Summary:
penelitian baru menunjukkan , Mungkin ada tumpang tindih antara variasi genetik langka terkait dengan gangguan bipolar dan mereka yang terlibat dalam skizofrenia dan autisme
penelitian baru menunjukkan , Mungkin ada tumpang tindih antara variasi genetik langka terkait dengan gangguan bipolar dan mereka yang terlibat dalam skizofrenia dan autisme
....................
Sebuah studi baru menunjukkan mungkin ada
tumpang tindih antara variasi genetik langka terkait dengan gangguan bipolar / bipolar disorder (BD) dan
mereka yang terlibat dalam skizofrenia dan autisme.
Penelitian ini dilakukan oleh para peneliti di
University of Iowa Carver College of Medicine, Johns Hopkins School of
Medicine, dan Cold Spring Harbor Laboratory dan diterbitkan baru-baru dalam
JAMA Psychiatry, menambah pemahaman yang berkembang bahwa banyak penyakit
kejiwaan berbagi akar genetik, tapi merupakan salah satu yang pertama menyarankan
tumpang tindih genetik antara gangguan bipolar dan autisme.
Gangguan bipolar adalah salah satu penyakit jiwa yang paling penting karena cukup umum - yang mempengaruhi antara 1 dan 3 persen dari populasi - dan cukup melemahkan. Meskipun banyak pasien dibantu oleh perawatan, seperti lithium, sekitar sepertiga dari orang yang terkena BD tidak melakukannya dengan baik dengan terapi saat ini. Meskipun itu lama diketahui bahwa gangguan bipolar sangat diwariskan, mengidentifikasi varian genetik tertentu yang berkontribusi terhadap penyakit telah terbukti sulit.
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Bipolar disorder
has genetic links to autism, study shows
Findings from a two-pronged approach add to evidence of shared genetic
susceptibility across major psychiatric disorders
Date:
May 4, 2016
Source:
University of Iowa
Health Care
Summary:
There may be an overlap between rare
genetic variations linked to bipolar disorder and those implicated in
schizophrenia and autism, new research suggests.
....................
A new study suggests there may be an overlap between rare genetic
variations linked to bipolar disorder (BD) and those implicated in
schizophrenia and autism.
The study, by researchers at the University of Iowa Carver College of
Medicine, Johns Hopkins School of Medicine, and Cold Spring Harbor Laboratory
and published recently in JAMA Psychiatry, adds to the growing
understanding that many psychiatric diseases share genetic roots, but is among
the first to suggest a genetic overlap between bipolar disorder and autism.
Bipolar disorder is one of the most important psychiatric illnesses because
it is fairly common -- affecting between 1 and 3 percent of the population --
and quite debilitating. Although many patients are helped by treatments, such
as lithium, about one third of people affected by BD do not do well with
current therapies. Although it's long been known that bipolar disorder is
highly heritable, identifying specific genetic variants that contribute to the
illness has proven difficult.
Within the last decade, advances in human genome studies have helped
uncover several so-called common variations, but none of these variations alone
have a large effect. Even more recently, the advent of rapid and relatively
cheap next-generation gene sequencing technology has provided an opportunity to
find rare variations that might individually have a large effect.
"Common variations are thought to each individually have only a tiny
impact -- for example, increasing a person's likelihood of getting a disease by
10 to 20 percent," says James Potash, MD, UI professor and DEO of
psychiatry, and senior author of the new study. "The hope with rare
variations is that they individually have a much bigger impact, like doubling
or quadrupling risk for disease."
Potash and his colleagues devised a two-pronged strategy, combining a
case-control approach with family-based exome sequencing to maximize their
chances of identifying rare variants that contribute to BD.
The idea behind the case-control approach is simple: if a genetic variant
is found more often in the group of individuals who have the disease compared
to a control group of people without the condition, then the gene variation
might be associated with increasing susceptibility to the disease. Very large
datasets are key to the success of this approach.
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Ide di balik pendekatan kasus kontrol sederhana
: jika varian genetik ditemukan lebih sering pada kelompok individu yang
memiliki penyakit dibandingkan dengan kelompok kontrol dari orang tanpa kondisi
, maka variasi gen mungkin terkait dengan peningkatan kerentanan terhadap
penyakit.dataset sangat besar adalah kunci untuk keberhasilan
pendekatan ini .
Exome sequencing of families affected by a disease is more sophisticated.
Comparing exome sequences of related individuals, affected and unaffected by
BD, can distinguish variants that "travel with" or segregate with the
disease. This approach has long been used to identify gene variants or
mutations that are passed from parents to children that cause disease.
Overall the family study identified 84 rare variants (in 82 genes) that
segregated with BD and that were also predicted to be damaging to the proteins
encoded by those genes. The team then tested the likelihood that these rare
variations might be involved in causing BD by looking for them in three large
case-control datasets that included genome sequences from a total of 3,541
individuals with BD and 4,774 control patients.
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Secara keseluruhan studi keluarga diidentifikasi 84 varian langka ( di 82 gen ) yang dipisahkan dengan BD dan yang juga diprediksi akan merusak protein yang dikodekan oleh gen mereka . Tim kemudian menguji kemungkinan bahwa variasi langka mungkin terlibat dalam menyebabkan BD dengan mencari mereka di tiga dataset kasus - kontrol besar yang termasuk urutan genom dari total 3.541 individu dengan BD dan 4.774 pasien kontrol .
Despite the relatively large size of the combined datasets, the approach
was not powerful enough to identify any of the individual rare variants as
definitively associated with BD. However, 19 genes stood out as being
over-represented in BD cases compared to controls.
"The results were not strong enough for us to say 'we have pinpointed
the genetic culprits.' But it was strong enough for us to remain interested in
these genes as potential contributors to bipolar disorder," says Potash,
who also is the Paul W. Penningroth Professor and Chair of Psychiatry and a
member of the Pappajohn Biomedical Institute at the UI.
However, when the team considered the 19 genes as a group, they realized
that several were also members of groups of genes that had been implicated in
autism and schizophrenia.
"It turned out that the schizophrenia and the autism genes were all more
represented among our 82 genes than you would expect by chance," Potash
says. "And when we looked at our whittled down group of 19 genes, the
autism genes continued to be unexpectedly prominent among them.
"With studies like this we are finally, after decades of effort,
making real progress in nailing down groups of genes and variations in them
that play a role in causing bipolar disorder," Potash adds. "The
mechanistic insights we gain from identifying associated genes we hope will
point us in the direction of developing new treatments to make a difference for
the many people affected by this illness.
Story Source:
The above post is reprinted from materials provided byUniversity of
Iowa Health Care. Note: Materials may be edited for
content and length.
Journal Reference:
1.
Fernando S. Goes, Mehdi Pirooznia, Jennifer S. Parla, Melissa Kramer, Elena
Ghiban, Senem Mavruk, Yun-Ching Chen, Eric T. Monson, Virginia L. Willour,
Rachel Karchin, Matthew Flickinger, Adam E. Locke, Shawn E. Levy, Laura J.
Scott, Michael Boehnke, Eli Stahl, Jennifer L. Moran, Christina M. Hultman,
Mikael Landén, Shaun M. Purcell, Pamela Sklar, Peter P. Zandi, W. Richard
McCombie, James B. Potash. Exome Sequencing of Familial Bipolar
Disorder. JAMA Psychiatry, 2016; DOI:10.1001/jamapsychiatry.2016.0251
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