Summary

Andrew Mammen, M.D., Ph.D., joined the NIAMS in 2014 to lead the Muscle Disease Unit in the Laboratory of Muscle Stem Cells and Gene Regulation. He obtained his medical degree and Ph.D. in neuroscience at Johns Hopkins in 2000, where he subsequently completed his medicine internship, neurology residency, and neuromuscular fellowship. Before his appointment at the NIH, Dr. Mammen was an Associate Professor of Neurology and Medicine at the Johns Hopkins University School of Medicine. He co-founded the Johns Hopkins Myositis Center in 2007, where he continues to see myositis patients as an adjunct faculty member. Dr. Mammen and his colleagues at Hopkins discovered a novel form of autoimmune myopathy associated with statin use and autoantibodies recognizing HMG-CoA reductase, the pharmacologic target of statins. 

In addition to clinical studies involving myositis patients, his current laboratory research interests include defining pathogenic mechanisms in the various forms of autoimmune myopathy and understanding the role of myositis autoantigens in muscle regeneration.

Research Statement

Dr. Mammen's research focuses on myositis, a rare family of autoimmune diseases in which the body's immune system attacks healthy muscle tissue, causing inflammation, weakness, fatigue, and pain in skeletal muscles. Myositis is often accompanied by problems that affect the skin, lungs, and joints. In particular, his team studies dermatomyositis, which can include a skin rash; the anti-synthetase syndrome, which can include rash, lung disease, and arthritis; inclusion-body myositis, which typically affects the muscles of older adults; and immune-mediated necrotizing myopathy, which can cause especially severe weakness in children and adults alike.

When he was on the faculty at Johns Hopkins, Dr. Mammen co-founded the Johns Hopkins Myositis Center in 2007. He and his Hopkins colleagues discovered a form of immune-mediated necrotizing myopathy triggered by statins, a medication used to lower cholesterol concentrations (Arthritis Rheum 63:713–721, 2011). This disease occurs in approximately 1 in 50,000 black and white Americans exposed to statins. However, working with colleagues in New Mexico, he found that members of the Navajo Nation are much more likely to develop this disease (Arthritis Rheum 2022; DOI:10.1002/art.42126; online ahead of print). Indeed, approximately 1 in 300 of these American Indians may develop this form of myositis if exposed to statins. Dr. Mammen's lab is currently trying to understand why some people can safely use statins while others are at an increased risk of developing myositis and should avoid this cholesterol-lowering medication.

At the NIH, Dr. Mammen's lab is 

1) defining the different subtypes of autoimmune muscle disease based on muscle histology, autoantibodies, and other biomarkers. 

2) elucidating the role of myositis autoantibodies in the pathogenesis of myositis.

3) developing animal models of myositis that are relevant to human diseases.

4) understanding how environmental exposures, including medications such as statins and cancer immunotherapies, can trigger autoimmune muscle disease.

5) using novel therapeutic strategies to treat myositis patients at the NIH Clinical Center.

In addition to seeing myositis patients at the NIH Clinical Center, Dr. Mammen is an adjunct professor of neurology and medicine at Hopkins, where he continues to see patients at the Myositis Center.

Scientific Publications

Increased risk of statin-associated autoimmune myopathy among American Indians.

Wei J, Ketner E, Mammen AL
Arthritis Rheumatol.
2022 Sep;
74(9).
doi: 10.1002/art.42126
PMID: 35333459

The phenotype of myositis patients with anti-Ku autoantibodies.

Casal-Dominguez M, Pinal-Fernandez I, Derfoul A, Graf R, Michelle H, Albayda J, Tiniakou E, Adler B, Danoff SK, Lloyd TE, Christoper-Stine L, Paik JJ, Mammen AL
Semin Arthritis Rheum.
2021 Aug;
51(4).
doi: 10.1016/j.semarthrit.2021.04.012
PMID: 34144382

Anti-mitochondrial autoantibodies are associated with cardiomyopathy, dysphagia, and features of more severe disease in adult-onset myositis.

Sabbagh SE, Pinal-Fernandez I, Casal-Dominguez M, Albayda J, Paik JJ, Miller FW, Rider LG, Mammen AL, Christopher-Stine L, Johns Hopkins Myositis Center Group
Clin Rheumatol.
2021 Oct;
40(10).
doi: 10.1007/s10067-021-05730-7
PMID: 33851273

The composition of cellular infiltrates in anti-HMG-CoA reductase-associated myopathy.

Chung T, Christopher-Stine L, Paik JJ, Corse A, Mammen AL
Muscle Nerve.
2015 Aug;
52(2).
doi: 10.1002/mus.24642
PMID: 25737145

Cytosolic 5'-Nucleotidase 1A As a Target of Circulating Autoantibodies in Autoimmune Diseases.

Lloyd TE, Christopher-Stine L, Pinal-Fernandez I, Tiniakou E, Petri M, Baer A, Danoff SK, Pak K, Casciola-Rosen LA, Mammen AL
Arthritis Care Res (Hoboken).
2016 Jan;
68(1).
doi: 10.1002/acr.22600
PMID: 25892010

The Prevalence of Individual Histopathologic Features Varies according to Autoantibody Status in Muscle Biopsies from Patients with Dermatomyositis.

Pinal-Fernandez I, Casciola-Rosen LA, Christopher-Stine L, Corse AM, Mammen AL
J Rheumatol.
2015 Aug;
42(8).
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