Research on aging, longevity, and senescence has become an increasingly important field in the quest to extend human health- and lifespan. Although these terms are related, they are distinct concepts in biology:
Aging refers to the progressive physiological changes in an organism that lead to a decline in biological functions and increased vulnerability to stress and disease over time. It is a general process that occurs throughout the adult life of living organisms. Aging is the primary risk factor for most neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). As the population ages, the prevalence of these conditions continues to increase.
Longevity refers to living a longer and healthier life, encompassing both the length of one’s lifespan and the quality of health during those years. It’s not just about extending life expectancy, but also about maintaining mental and physical fitness well into old age. To better understand longevity, researchers have turned to aging clocks, which use molecular markers, such as DNA methylation patterns, to estimate biological age. These epigenetic changes accumulate over time and reflect the impact of lifestyle, environmental factors, and genetic predisposition on aging and can be investigated in preclinical animal models.
Senescence, while often used interchangeably with aging, specifically refers to the cellular mechanisms of biological aging. It describes the loss of cells ability to divide while remaining metabolically active. Senescence occurs at the cellular level and contributes to the overall aging process of an organism. Ex vivo, senescence can be evaluated by measuring β-galactosidase activity.
In Vitro Models of Senescence
In vitro models of cellular senescence have become essential tools for studying the mechanisms of aging and age-related diseases. These models provide a controlled environment to induce and analyze senescence in various cell types. Additionally, mitochondria and reactive oxygen species (ROS) play crucial roles in cellular aging and senescence and can be selectively assessed using various in vitro approaches.
Video: Representative video of oxidative stress in primary cortical mouse neurons after BSO treatment. ROS accumulation visualized with CellROX™ Deep Red Reagent.
Rodent Models of Aging
Our diverse range of rodent models, including aged mice and rats, Senescence-Accelerated Mouse-Prone (SAMP) strains, and models for neurodegenerative, metabolic, and inflammatory diseases, are essential tools for studying healthy as well as pathological aging. Selecting the most appropriate model is crucial for addressing your specific research questions. Contact us today to select the optimal solution for your research needs.
Modelling Cognitive Impairment
While cognitive changes are a physiological part of aging, significant decline can impact daily life and may indicate pathological conditions, such as dementia. SAMP8 mice are an excellent model for studying cognitive impairment in both pathological and healthy aging due to their accelerated aging process, which leads to early cognitive decline (Figure 1).
Figure 1: Cognitive impairment of SAMP8 mice. SAMP8 mice were evaluated for learning deficits in the contextual fear conditioning test at the age of 4 months compared to SAMR1 mice of the same age as physiologically aging control mice. Mean freezing duration for 5 minutes after receiving the foot shock. Mean + SEM, n = 12 per group, unpaired t-test, ***p <0.001.
Modelling Motor Impairment
SAMP8 mice are not only useful for research aimed at cognitive decline but also to model age-related changes in motor function. These impairments are valuable for aging research as they mimic the motor decline observed in elderly humans. SAMP8 mice allow to evaluate the mechanisms underlying motor deterioration that consequently can lead to the discovery of potential biomarkers. Furthermore, SAMP8 mice allow testing interventions that are aimed at improving motor function in aging populations (Figure 2).
Figure 2: Motor deficits in SAMP8 mice. SAMP8 mice were evaluated for motor deficits in the wire hanging test at the age of 4 months compared to SAMR1 mice of the same age as physiologically aging control mice. Wire hanging time in seconds. 300 seconds cut-off time. Mean + SEM, n = 12 per group, unpaired t-test, *p <0.05.
Modelling the Metabolic Syndrome
Metabolic dysregulation is a hallmark of aging and plays a crucial role in the development of age-related diseases. This complex interplay between metabolism and aging affects multiple biological processes and tissues throughout the body. To model obesity in vivo, Scantox offers the streptozotocin-treated mouse model that can further be fed with high-fat diet to amplify the phenotype.
Modelling Inflammation
Inflammation plays a crucial role in the aging process and the development of age-related diseases. This phenomenon, often referred to as “inflammaging” is characterized by chronic, low-grade inflammation that persists in older individuals.
Inflammation can be modelled by various preclinical in vitro and in vivo models. Furthermore, aged transgenic mouse models, such as 5xFAD mice can be used to model inflammation (Figure 3).
Figure 3: Inflammation in aged 5xFAD mice. IL-1β (A) and MCP1 (B) levels in 3 and 7 months old 5xFAD mice as evaluated by immunosorbent assay (MesoScale Discovery). Mean + SEM, n = 16, Mann-Whitney test, ***p <0.001.
Scantox offers a custom-tailored study design for your aging study, and we are flexible to accommodate to your special interests. We are also happy to advice you and propose study designs.
We would be happy to test your compounds in these preclinical in vitro and in vivo models of aging! Readouts depend on the model but the most common are:
We are happy to receive your inquiry.
