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Ole B. Suhr

Bio: Ole B. Suhr is an academic researcher from Umeå University. The author has contributed to research in topics: Transthyretin & Amyloidosis. The author has an hindex of 53, co-authored 241 publications receiving 11567 citations. Previous affiliations of Ole B. Suhr include Karolinska Institutet & Kumamoto University.


Papers
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Journal ArticleDOI
TL;DR: Patisiran improved multiple clinical manifestations of hereditary transthyretin amyloidosis with polyneuropathy and showed an effect on gait speed and modified BMI.
Abstract: BACKGROUND: Patisiran, an investigational RNA interference therapeutic agent, specifically inhibits hepatic synthesis of transthyretin.METHODS: In this phase 3 trial, we randomly assigned patients ...

1,671 citations

Journal ArticleDOI
TL;DR: A therapeutic approach mediated by RNA interference (RNAi) could reduce the production of transthyretin in peripheral nerves and the heart as mentioned in this paper, which is caused by the deposition of hepatocyte-derived tranthymretin amyloid in peripheral nerve and heart.
Abstract: BACKGROUND: Transthyretin amyloidosis is caused by the deposition of hepatocyte-derived transthyretin amyloid in peripheral nerves and the heart. A therapeutic approach mediated by RNA interference (RNAi) could reduce the production of transthyretin. METHODS: We identified a potent antitransthyretin small interfering RNA, which was encapsulated in two distinct first- and second-generation formulations of lipid nanoparticles, generating ALN-TTR01 and ALN-TTR02, respectively. Each formulation was studied in a single-dose, placebo-controlled phase 1 trial to assess safety and effect on transthyretin levels. We first evaluated ALN-TTR01 (at doses of 0.01 to 1.0 mg per kilogram of body weight) in 32 patients with transthyretin amyloidosis and then evaluated ALN-TTR02 (at doses of 0.01 to 0.5 mg per kilogram) in 17 healthy volunteers. RESULTS: Rapid, dose-dependent, and durable lowering of transthyretin levels was observed in the two trials. At a dose of 1.0 mg per kilogram, ALN-TTR01 suppressed transthyretin, with a mean reduction at day 7 of 38%, as compared with placebo (P=0.01); levels of mutant and nonmutant forms of transthyretin were lowered to a similar extent. For ALN-TTR02, the mean reductions in transthyretin levels at doses of 0.15 to 0.3 mg per kilogram ranged from 82.3 to 86.8%, with reductions of 56.6 to 67.1% at 28 days (P<0.001 for all comparisons). These reductions were shown to be RNAi-mediated. Mild-to-moderate infusion-related reactions occurred in 20.8% and 7.7% of participants receiving ALN-TTR01 and ALN-TTR02, respectively. CONCLUSIONS: ALN-TTR01 and ALN-TTR02 suppressed the production of both mutant and nonmutant forms of transthyretin, establishing proof of concept for RNAi therapy targeting messenger RNA transcribed from a disease-causing gene. (Funded by Alnylam Pharmaceuticals; ClinicalTrials.gov numbers, NCT01148953 and NCT01559077.).

816 citations

Journal ArticleDOI
TL;DR: This study provides Class II evidence that 20 mg tafamidis QD was associated with no difference in clinical progression in patients with TTR-FAP, as measured by the NIS-LL and the Norfolk QOL-DN score, supporting the hypothesis that preventing TTR dissociation can delay peripheral neurologic impairment.
Abstract: Objectives: To evaluate the efficacy and safety of 18 months of tafamidis treatment in patients with early-stage V30M transthyretin familial amyloid polyneuropathy (TTR-FAP). Methods: In this rando ...

626 citations

Journal ArticleDOI
25 Dec 2013-JAMA
TL;DR: Among patients with familial amyloid polyneuropathy, the use of diflunisal compared with placebo for 2 years reduced the rate of progression of neurological impairment and preserved quality of life.
Abstract: RESULTS By multiple imputation, the NIS+7 score increased by 25.0 (95% CI, 18.4-31.6) points in the placebo group and by 8.7 (95% CI, 3.3-14.1) points in the diflunisal group, a difference of 16.3 points (95% CI, 8.1-24.5 points; P < .001). Mean SF-36 physical scores decreased by 4.9 (95% CI, −7.6 to −2.2) points in the placebo group and increased by 1.5 (95% CI, −0.8 to 3.7) points in the diflunisal group (P < .001). Mean SF-36 mental scores declined by 1.1 (95% CI, −4.3 to 2.0) points in the placebo group while increasing by 3.7 (95% CI, 1.0-6.4) points in the diflunisal group (P = .02). By responder analysis, 29.7% of the diflunisal group and 9.4% of the placebo group exhibited neurological stability at 2 years (<2-point increase in NIS+7 score; P = .007). CONCLUSIONS AND RELEVANCE Among patients with familial amyloid polyneuropathy, the use of diflunisal compared with placebo for 2 years reduced the rate of progression of neurological impairment and preserved quality of life. Although longer-term follow-up studies are needed, these findings suggest benefit of this treatment for familial amyloid polyneuropathy.

539 citations

Journal ArticleDOI
TL;DR: Liver transplantation does have important benefits in FAP during the first 2 years after surgery, Neurological decline is halted and amyloid deposits can be mobilised.

530 citations


Cited by
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Journal ArticleDOI
TL;DR: Authors/Task Force Members: Piotr Ponikowski* (Chairperson) (Poland), Adriaan A. Voors* (Co-Chair person) (The Netherlands), Stefan D. Anker (Germany), Héctor Bueno (Spain), John G. F. Cleland (UK), Andrew J. S. Coats (UK)

13,400 citations

Journal ArticleDOI
06 Jun 1986-JAMA
TL;DR: The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or her own research.
Abstract: I have developed "tennis elbow" from lugging this book around the past four weeks, but it is worth the pain, the effort, and the aspirin. It is also worth the (relatively speaking) bargain price. Including appendixes, this book contains 894 pages of text. The entire panorama of the neural sciences is surveyed and examined, and it is comprehensive in its scope, from genomes to social behaviors. The editors explicitly state that the book is designed as "an introductory text for students of biology, behavior, and medicine," but it is hard to imagine any audience, interested in any fragment of neuroscience at any level of sophistication, that would not enjoy this book. The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or

7,563 citations

Journal ArticleDOI
TL;DR: The Society of Echocardiography (SEDC) is an educational activity for cardiovascular physicians and cardiac sonographers with a knowledge base in the field of echo-cardiography as discussed by the authors.
Abstract: on Statement: Society of Echocardiography is accreditedby theAccreditationCouncil for edical Education to provide continuingmedical education for physicians. n Society of Echocardiography designates this educational activity for of 1.0 AMA PRA Category 1 Credits . Physicians should only claim credit te with the extent of their participation in the activity. CCI recognize ASE’s certificates and have agreed to honor the credit hours registry requirements for sonographers. Society of Echocardiography is committed to ensuring that its educational ll sponsored educational programs are not influencedby the special interests ation or individual, and itsmandate is to retain only those authors whose fists canbeeffectively resolved tomaintain thegoals andeducational integrity y. While a monetary or professional affiliation with a corporation does not fluence an author’s presentation, the Essential Areas and policies of the ire that any relationships that could possibly conflict with the educational activity be resolved prior to publication and disclosed to the audience. f faculty and commercial support relationships, if any, have been indicated. ience: is designed for all cardiovascular physicians and cardiac sonographers with erest and knowledge base in the field of echocardiography; in addition, reschers, clinicians, intensivists, and other medical professionals with a spein cardiac ultrasound will find this activity beneficial.

5,151 citations

Journal ArticleDOI
01 Jan 2014
TL;DR: This activity is designed for all cardiovascular physicians and cardiac sonographers with arest and knowledge base in the field of echocardiography and reschers, clinicians, intensivists, and other medical professionals with a spein cardiac ultrasound will find this activity beneficial.
Abstract: on Statement: Society of Echocardiography is accredited by the Accreditation Council for edical Education to provide continuing medical education for physicians. n Society of Echocardiography designates this educational activity for of 1.0 AMA PRA Category 1 Credits . Physicians should only claim credit te with the extent of their participation in the activity. CCI recognize ASE’s certificates and have agreed to honor the credit hours registry requirements for sonographers. Society of Echocardiography is committed to ensuring that its educational ll sponsored educational programs are not influenced by the special interests ation or individual, and its mandate is to retain only those authors whose fists can be effectively resolved to maintain the goals andeducational integrity y. While a monetary or professional affiliation with a corporation does not fluence an author’s presentation, the Essential Areas and policies of the ire that any relationships that could possibly conflict with the educational activity be resolved prior to publication and disclosed to the audience. f faculty and commercial support relationships, if any, have been indicated. ience: is designed for all cardiovascular physicians and cardiac sonographers with erest and knowledge base in the field of echocardiography; in addition, reschers, clinicians, intensivists, and other medical professionals with a spein cardiac ultrasound will find this activity beneficial.

4,739 citations

Journal ArticleDOI
TL;DR: By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.

4,319 citations