Biology of Healthy Aging Program

Studies within this group range from molecular and cellular to genetic and laboratory animal-based approaches targeted to understanding the mechanisms, risk factors, and pathophysiology of aging-related changes in health, function, and quality of life.

In addition, the faculty and staff involved in this interdisciplinary program has considerable expertise in the development of clinical translational studies in human populations, epidemiological studies in populations of older adults, and in clinical intervention trials.

The major aims of the Biology of Healthy Aging Program

  1. Investigate etiologies for age-related activation in inflammatory and renin-angiotensin system pathways and their consequences on the development of frailty, sarcopenia, cognitive decline, osteopenia, and other chronic diseases of older adults.

  2. Develop treatments that focus on inflammation and angiotensin system activation and their consequences.

  3. Investigate the viral-related causes and treatments for immunosenescence in older adults, and develop treatments for these etiologies.

  4. Develop novel vaccination strategies for frail older adults for influenza and CMV.

  5. Study the etiologies and consequences of aging-related changes in mitochondria on health and well being.

  6. Develop and validate physiotypes of frailty and robust health in older adults by integrating genetic, cellular, and clinical level phenomena into integrative biological models

  7. Translate novel aging-related biological findings into diagnostic tests, novel treatments, and preventive strategies that will help to optimize quality of life and healthy aging.


Our Team

Our Faculty

Peter Magdy Abadir, M.D.

Associate Professor of Medicine

Peter Magdy Abadir

Tae Hwan Chung, M.D.

Assistant Professor of Physical Medicine and Rehabilitation
Assistant Professor of Neurology

Tae Hwan Chung

Neal S. Fedarko, Ph.D.

Director, Clinical Research Core Laboratory, Institute for Clinical & Translational Research
Co-Director, Fellowship Training Program in Gerontology and Geriatrics
Co-Director, Biology of Healthy Aging Program, Johns Hopkins School of Medicine
Professor of Medicine

Neal S. Fedarko

Sean Xiao Leng, M.D., Ph.D.

Professor of Medicine

Sean Xiao Leng

Lolita Sai Nidadavolu, M.D., Ph.D.

Assistant Professor of Medicine

Lolita Sai Nidadavolu, M.D., Ph.D.

Esther Seunghee Oh, M.D., Ph.D.

Co-Director, Johns Hopkins Memory and Alzheimer's Treatment Center
Associate Professor of Medicine
Assistant Professor of Pathology
Joint Appointment in Psychiatry and Behavioral Sciences

Esther Seunghee Oh

Jeremy David Walston, M.D.

Raymond and Anna Lublin Professor of Geriatric Medicine & Gerontology
Deputy Director, Division of Geriatric Medicine and Gerontology
Co-Director, Biology of Healthy Aging Program
Professor of Medicine
Professor of Oncology

Jeremy David Walston

Reyhan Marcus Westbrook, Ph.D.

Assistant Professor of Medicine

Reyhan Marcus Westbrook

Our Fellows

Mariann Gabrawy


Gizem Keceli


Thomas Laskow, M.D.

Thomas Laskow

Geoffrey Shimberg


Our Research

The Aging Renin Angiotensin System

Renin Angiotensin System

The Renin Angiotensin System (RAS) is a major hormone system with a crucial role in physiologic and pathophysiologic mechanisms in almost every organ system, including brain, liver, kidney, bones, heart, and blood vessels. It is regarded as a key regulator of hypertension, cardiovascular disease, and renal function. Evidence strongly supports that Angiotensin II (Ang II) promotes inflammation and the generation of reactive oxygen species and governs the onset and progression of vascular senescence, which are all associated with the functional and structural changes that lead to age-related diseases. 

Chronic Inflammation and Late-Life Decline

Chronic Inflammation

The importance of age-related, low-level chronic elevations in inflammatory cytokines is increasingly recognized as pathophysiologic in older adults. This chronic inflammatory state has adverse effects on multi-organ systems, leading to the development of chronic diseases, disability, frailty, and mortality in older adults.

Immune Senescence

Immune Senescence

Immune senescence, or the aging of the immune system, particularly its effect on changes in lymphocyte development and function, predisposes older adults to a higher risk of latent virus reactivation. The varicella-zoster virus, for example, the agent responsible for chickenpox in children, remains dormant in nerve cells in the trigeminal and dorsal root ganglia and reactivates in later life to cause shingles and post-herpetic neuralgia.

Other persistent viral infections include Epstein-Barr virus, herpes simplex virus-1 and -2, and cytomegalovirus (CMV).

Age-related immune senescent remodeling likely involves both the innate and adaptive immune system and may contribute to the immune system’s functional decline; chronic inflammatory state; and risk for frailty, chronic disease, and functional decline in older adults.

Mitochondrial Biology

Aged Brain

Mitochondria are the cells’ powerhouses and play a crucial role in the development of increased levels of oxidative stress and ultimately in program cell death (apoptosis). Investigators focused on aging have long hypothesized that mitochondria are of crucial importance to the evolution of aging and frail phenotypes.

Muscle and Bone Biology in Frailty

Muscle and Bone

Decreases in physical stature and mobility, which reflect changes in the scaffolding and leveraging systems of the body-the skeleton and muscles, are two easily observed changes associated with aging. Bone and muscle are dynamic organs that undergo continuous repair and remodeling throughout life. These two systems are inter-related because the action of muscle on bone is key to normal remodeling of bone and muscle mass is influenced by bone density.

Persistent Viral Infections and T-Cell Repertoires in Older Adults

In older adults, persistent infections caused by herpes viruses can be a common problem. These viruses usually enter the hosts, cause primary disease earlier in life, and remain latent in various cell types. Under the appropriate conditions, these viruses may reactivate to cause disease and elicit recall responses from the adaptive immune system, resulting in inflammation and proliferation of antigen-specific T-cells aimed at suppressing viral replication. 

Reactivation of the herpes viruses is more common in immunosuppressed or immunocompromised people who have impaired T-cell immunity, such as transplant recipients and patients infected with the human immunodeficiency virus (HIV).

Human cytomegalovirus (CMV) infects more than 80 percent of adults 60 years and older in the United States. After an acute infection that may produce anywhere from no symptoms in young healthy adults to severe congenital syndromes in newborns, CMV remains latent in mononuclear cells, among other cell types, in a nonreplicating or slowly replicating form.

In immunocompromised patients, CMV is the most common opportunistic pathogen to cause significant morbidity and mortality, reactivating frequently and producing severe disease. However, the long-term clinical effect of CMV infection in people with a competent immune system is not well known. Cardiovascular disease has been associated with CMV seropositivity in adults.