F. Hoffmann-La Roche AG

Switzerland

About Roche

Roche is a global pioneer in pharmaceuticals and diagnostics focused on advancing science to improve people’s lives. The combined strengths of pharmaceuticals and diagnostics under one roof have made Roche the leader in personalised healthcare – a strategy that aims to fit the right treatment to each patient in the best way possible.

Roche is the world’s largest biotech company, with truly differentiated medicines in oncology, immunology, infectious diseases, ophthalmology and diseases of the central nervous system. Roche is also the world leader in in vitro diagnostics and tissue-based cancer diagnostics, and a frontrunner in diabetes management.

Founded in 1896, Roche continues to search for better ways to prevent, diagnose and treat diseases and make a sustainable contribution to society. The company also aims to improve patient access to medical innovations by working with all relevant stakeholders. Thirty medicines developed by Roche are included in the World Health Organization Model Lists of Essential Medicines, among them life-saving antibiotics, antimalarials and cancer medicines. Roche has been recognised as the Group Leader in sustainability within the Pharmaceuticals, Biotechnology & Life Sciences Industry nine years in a row by the Dow Jones Sustainability Indices (DJSI).

The Roche Group, headquartered in Basel, Switzerland, is active in over 100 countries and in 2017 employed about 94,000 people worldwide. In 2017, Roche invested CHF 10.4 billion in R&D and posted sales of CHF 53.3 billion. Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit www.roche.com.

1 December 2017 - 30 November 2018

Region: Global
Subject/journal group: All

The table to the right includes counts of all research outputs for F. Hoffmann-La Roche AG published between 1 December 2017 - 30 November 2018 which are tracked by the Nature Index.

Hover over the donut graph to view the FC output for each subject. Below, the same research outputs are grouped by subject. Click on the subject to drill-down into a list of articles organized by journal, and then by title.

Note: Articles may be assigned to more than one subject area.

AC	FC
129	53.68

Outputs by subject (FC)

Subject	AC	FC
Chemistry	27	13.11
Life Sciences	107	42.26
Cancer Cell	4	1.71
Cancer Research	2	0.54
Cell	3	0.92
Cell Metabolism	1	1
Cell Stem Cell	2	0.07
Developmental Cell	1	0.07
Genome Research	2	0.29
Journal of Biological Chemistry	8	2.27
Journal of Cell Biology	1	1
Journal of Clinical Investigation	2	0.17
Journal of Experimental Medicine	5	3.10
Journal of Neuroscience	3	2.05
Molecular Cell	3	2.04
Nature	5	3.59
Nature Cell Biology	1	0.04
Nature Chemical Biology	1	0.94
Nature Communications	17	3.64
Nature Genetics	3	0.06
Nature Immunology	5	1.51
Nature Medicine	5	1.37
Nature Methods	1	0.95
Nature Neuroscience	1	0.05
Neuron	1	0.88
PLOS Biology	1	0.05
PLOS Genetics	1	0.87
Proceedings of the National Academy of Sciences of the United States of America	13	8.01
Science	2	0.06
Science Translational Medicine	6	2.43
The EMBO Journal	1	0.45
eLife	6	2.12
Physical Sciences	2	0.04

Highlight of the month

Lighting the synaptic pathway

An antibody drug that blocks part of the innate immune system in the brain can help prevent tau-induced loss of neuronal connections in mouse models of Alzheimer’s disease.

Working in mice that express a pathological form of human tau, researchers at the Roche subsidiary Genentech screened for proteins that build up on the receiving end of neuronal junctions. Alongside active forms of tau, they found high levels of C1q, part of the complement system that aids other immune processes.

Together, the two proteins seemed to tag the synapses for destruction by immune-scavenging cells called microglia. That synaptic removal could be blocked, however, by administering a C1q-directed antibody directly to the mouse brain. Five days after the injection, synaptic density was enhanced.

The findings suggest that targeting C1q and the microglial-mediated eating of synapses is worthwhile for treating Alzheimer’s and other neurodegenerative disorders.

Supported content