The Geropathology Research Network: An Interdisciplinary Approach for Integrating Pathology Into Research on Aging

Abstract

Geropathology is the study of aging and age-related lesions and diseases in the form of whole necropsies/autopsies, surgical biopsies, histology, and molecular biomarkers. It encompasses multiple subspecialties of geriatrics, anatomic pathology, molecular pathology, clinical pathology, and gerontology. In order to increase the consistency and scope of communication in the histologic and molecular pathology assessment of tissues from preclinical and clinical aging studies, a Geropathology Research Network has been established consisting of pathologists and scientists with expertise in the comparative pathology of aging, the design of aging research studies, biostatistical methods for analysis of aging data, and bioinformatics for compiling and annotating large sets of data generated from aging studies. The network provides an environment to promote learning and exchange of scientific information and ideas for the aging research community through a series of symposia, the development of uniform ways of integrating pathology into aging studies, and the statistical analysis of pathology data. The efforts of the network are ultimately expected to lead to a refined set of sentinel biomarkers of molecular and anatomic pathology that could be incorporated into preclinical and clinical aging intervention studies to increase the relevance and productivity of these types of investigations.

Keywords: Aging; Geropathology; Geropathology Research Network; Health span.; Healthy aging; Histopathology; Life-span; Molecular pathology.

Figure 1.

The Geropathology Research Network is driven by an interdisciplinary approach.

Figure 2.

The Molecular Pathology Working group is charged with prioritizing the use of potential surrogate aging molecules.

Figure 3.

Initial objectives of the Anatomic Pathology Working group.

Figure 4.

Increased exercise endurance is associated with decreased lung inflammation in 24-month-old mice expressing mitochondrial catalase (mCAT) compared to 6-month-old mice expressing m/CAT. Exercise endurance was assessed by distance ran over a three day period. Inflammation grade was the average total score (from 1–4) for macrophage infiltration, perivascular and peribronchiolar lymphocytes, and intravascular leukocytes. N = 4–6/cohort, p ≤ .05 for 24 mo cohorts.

Figure 5.

Protein kinase A (PKA) Cβ null mice are resistant to age-induced cardiac hypertrophy, N = 12, 24–26 mo of age. Echocardiography revealed that aged PKA Cβ null mice had significantly lower LVMI (left ventricular mass index; determined by left ventricular mass standardized to tibia length) than WT littermates, suggesting cardiac dysfunction. Hearts were found to be almost 25% heavier than those of mutants suggesting heart weight could be an indicator of cardiac dysfunction.