Lifespan Changes Research Articles

Complexity in Complementation: Understanding lifespan change in the verb complementation of individuals

Complexity in Complementation: Understanding lifespan change in the verb complementation of individuals

Life Span Changes of Coffee White Stem Borers, Xylotrechus quadripes (Coleoptera: Cerambycidae) in Response to Directed Homosexual and Heterosexual Interactions

Our study on coffee white stem borers, Xylotrechus quadripes investigated the influence of different sex-based clustering factors on beetle survivorship and life spans. Our experiments involved various groups, including individually isolated virgin males, individually isolated virgin females, groups of only males, groups of only females, and mixed-sex groups. First, survivorship reached 100% within the initial 15 days for all groups except for isolated virgin males. In contrast, the survivorship rates of both groups involving only virgin females and only virgin males ranged from 80% to 90% compared to the maximum survival duration. Notably, in scenarios with males in groups or mixed-gender groups, survival dropped to zero percent after 45 days. Our study also highlighted the comparable costs incurred by males engaging in both homosexual and heterosexual interactions. Males interacting with females and other males exhibited similar survival curves, displaying shorter median life spans compared to isolated virgin males, suggesting that both courting and mounting behaviors, regardless of the recipient's sex, might affect the life span of males. Furthermore, our research revealed that female-female interactions, while less costly than male-male interactions, still reduced survival periods in only the female group. These findings highlight the cost possibly associated with same-sex interactions and shed light on the dynamics of mating behaviors in this beetle. In conclusion, our findings underscore the significance of studying behavioral and life history traits in different environmental contexts. Social circumstances and ecological factors significantly influence sexual differences in lifespan and highlight the complexity of the interplay between reproductive strategies and survival rates in Xylotrechus quadripes.

Carbon Footprint of Wool at Cradle to Farm-Gate Stage in Victoria, Australia

The raw material acquisition stage of wool involves raising sheep and a large amount of input and output, resulting in substantial greenhouse gas emissions. To date, the research literature on wool carbon footprint is limited, and there is a lack of research on Victoria. These studies did not consider the influence of changes in weight and productive lifespan. This study aims to address this knowledge gap by calculating the wool carbon footprint in Victoria and improving the calculation method. In this article, 20,000 sheep in Victoria were investigated. The average weights of the sheep were obtained by curve fitting and calculating. Two scenarios with 5-year and 6-year productive lifespans were used to calculate the carbon footprint of merino wool by the mass allocation method, economic allocation method, and protein mass allocation method. Results revealed that the carbon footprint of wool for the 5-year and 6-year productive lifespans were 14.158–49.040 kg carbon dioxide equivalent (CO2-e)/kg wool and 16.743–52.882 kg CO2-e/kg wool. Rumination and excretion accounted for the largest proportion, followed by phosphate fertilizer, electricity, and potash fertilizer. The longer the productive lifespan and the heavier the sheep, the greater the greenhouse gas emissions from rumination and excretion, leading to a larger carbon footprint for wool. For the same productive lifespan, the economic allocation method produced the highest carbon footprint for wool compared to the mass allocation method, which produced the lowest carbon footprint. This study provides a reference for the subsequent carbon footprint accounting of wool from cradle to farm-gate and helps the wool industry save energy and reduce emissions.

Changes in Life Span as an Integral Response to the Immune Status of the Organism and the Activity of Mobile Elements

Changes in Life Span as an Integral Response to the Immune Status of the Organism and the Activity of Mobile Elements

Changes in Lifespan as an Integral Response to the Organism’s Immune Status and Mobile Elements Activity

One of the key goals in studying the molecular and genetic basis of many pathologies is to find triggers, which could positively influence the incidence of age-dependent diseases and the rate of aging in general. A possible cause of age-dependent degradation of the organism functions inducing aging is immunosenescence. It is known that the increased activity of mobile elements observed with age may not only affect the level of genome stability, but also play a crucial role in the development of immune response. At the same time, the pivotal role of the nervous system in controlling lifespan has long been proven, and recently it has been shown that components of the machinery that regulate mobile element activity do function in the nervous system, and their functioning affects the development of neurodegenerative diseases. This mini-review presents evidence for complex aging regulation by the nervous and immune systems, involving systems that control mobile element activity and proposes a hypothetical scheme for their joint impact on lifespan.

Plenary F: Timing of Influences on Brain and Cognition: a Lifespan Perspective

Abstract & Learning Objectives:Brain and cognition vary and change markedly across the lifespan. I use magnetic resonance imaging and cognitive data to show that while general age trends can be identified in brain and cognition, there are great individual differences through life, and these are influenced by several factors, including at early life stages. Hence, in some respects, aging starts in the womb. Recognizing and understanding the impact of early relative to later stage factors on neurocognitive lifespan differences, changes and aging is a major challenge. Adequately meeting this challenge is crucial both to understand the mechanisms at work early in life, and to identify what and how residual variance may be affected by later life factors. Thus, knowledge of the timing of influences on brain and cognition along the lifespan is needed to develop realistic plans for prevention and intervention to optimize brain and cognition at different ages. I discuss how example factors such as prenatal drug exposure, birth weight, genetics, education, income, and “baseline” general cognitive ability, as well as cognitive training interventions relate to differences and/or changes in the human brain along the lifespan.Example findings are drawn from the studies of the Center for Lifespan Changes in Brain and Cognition (LCBC), where we follow individuals ranging in age from 0 to 100 years. Our studies are in part linked to Norwegian registry data, including the Mother, Father and Child Cohort study (Moba), the Norwegian Twin Registry and the Medical Birth Registry. Linkage to registry data on normal variation of pre-and perinatal characteristics, as well as studies of groups with known early biomedical risk, such a prenatal drug exposure, enable investigation of the possible impact of neurodevelopmental factors on brain and cognitive function through the entire life course. I also discuss how genetically informed studies of brain and cognition sampling broader age spans may contribute to our understanding of the timing of influences. Selectivity of samples constitute a challenge to generalizability in all human research. I discuss how research across international databases can, beyond boosting power and detect consistency of effects, help us appreciate there are diverse associations of possible factors of influence on different groups. This is crucial, as we need to understand to what extent various factors’ association with brain and cognition are universal or cohort-specific, prior to mechanistic understanding. Thus, in this presentation, I will discuss how transdisciplinary, longitudinal, multi-method, and multi-cohort research can illuminate factors that may influence brain and cognition, and their potential timing, in a lifespan perspective.Upon conclusion of this course, learners will be able to:1.Recognize that differences in brain and cognition even at advanced age may reflect early life factors, rather than, or in addition to, differences in brain and cognitive change with age2.Describe consistency as well as diversity of factors’ (such as SES) associations with brain and cognition across cohorts of different age and origin.3.Evaluate differences in factors present early in life, including at birth (“different offset”) before attributing variance in brain and cognitive function to changes with age (“different slope”)

Regression-based normative data for the D-KEFS Color-Word Interference Test in Norwegian adults ages 20–85

Objective: The Delis-Kaplan Executive Function System (D-KEFS) Color-Word-Interference Test (CWIT; AKA Stroop test) is a widely used measure of processing speed and executive function. While test materials and instructions have been translated to Norwegian, only American age-adjusted norms from D-KEFS are available in Norway. We here develop norms in a sample of 1011 Norwegians between 20 and 85 years. We provide indexes for stability over time and assess demographic adjustments applying the D-KEFS norms. Method: Participants were healthy Norwegian adults from Center for Lifespan Changes in Brain and Cognition (LCBC) (n = 899), the Dementia Disease Initiation (n = 77), and Oslo MCI (n = 35). Using regression-based norming, we estimated linear and non-linear effects of age, education, and sex on the CWIT 1-4 subtests. Stability over time was assessed with intraclass correlation coefficients (ICC). The normative adjustment of the D-KEFS norms was assessed with linear regression models. Results: Increasing age was associated with slower completion on all CWIT subtests in a non-linear fashion (accelerated lowering of performance with older age). Women performed better on CWIT-1&3. Higher education predicted faster completion time on CWIT-3&4. The original age-adjusted norms from D-KEFS did not adjust for sex or education. Furthermore, we observed significant, albeit small effects of age on all CWIT subtests. ICC analyses indicated moderate to good stability over time. Conclusion: We present demographically adjusted regression-based norms and stability indexes for the D-KEFS CWIT subtests. US D-KEFS norms may be inaccurate for Norwegians with high or low educational attainment, especially women.

Using Geospatial Analysis to Guide Marsh Restoration in Chesapeake Bay and Beyond

Coastal managers are facing imminent decisions regarding the fate of coastal wetlands, given ongoing threats to their persistence. There is a need for objective methods to identify which wetland parcels are candidates for restoration, monitoring, protection, or acquisition due to limited resources and restoration techniques. Here, we describe a new spatially comprehensive data set for Chesapeake Bay salt marshes, which includes the unvegetated-vegetated marsh ratio, elevation metrics, and sediment-based lifespan. Spatial aggregation across regions of the Bay shows a trend of increasing deterioration with proximity to the seaward boundary, coherent with conceptual models of coastal landscape response to sea-level rise. On a smaller scale, the signature of deterioration is highly variable within subsections of the Bay: fringing, peninsular, and tidal river marsh complexes each exhibit different spatial patterns with regards to proximity to the seaward edge. We then demonstrate objective methods to use these data for mapping potential management options on to the landscape, and then provide methods to estimate lifespan and potential changes in lifespan in response to restoration actions as well as future sea level rise. We account for actions that aim to increase sediment inventories, revegetate barren areas, restore hydrology, and facilitate salt marsh migration into upland areas. The distillation of robust geospatial data into simple decision-making metrics, as well as the use of those metrics to map decisions on the landscape, represents an important step towards science-based coastal management.

Sociosexual Exposure Has Opposing Effects on Male and Female Actuarial Senescence in the Fruit Fly Drosophila melanogaster.

Males and females rarely express the same length of life. Here, we studied how sociosexual exposure shapes male and female age-specific mortality rates in Drosophila melanogaster. We maintained focal females and males within large, replicated cohorts throughout life with individuals of the same or opposite sex. Consistent with previous works, we found that females kept throughout their lives with males had only half the lifespan of those maintained throughout life at the same density in same-sex cohorts. In contrast, only a small lifespan decrease was observed in the corresponding male treatments and the reduction in male lifespan following exposure throughout life to other males or females was similar. Deconvolution of underlying aging parameters revealed that changes in lifespan were underpinned by opposing effects on actuarial aging in males versus females. Exposure to the opposite or same sex increased initial mortality rate in both sexes. However, in females, increasing exposure to males increased the rate of aging, while increasing exposure to females actually decreased it. The effects were in the opposite direction in males and were much smaller in magnitude. Overall, the findings were consistent with reports suggesting that exposure to the same versus opposite sex can affect survival differently in males and females. However, they also reveal a new insight-that overall lifespan can be underpinned by key differences in actuarial senescence in each sex. The findings suggest that responses to same or opposite sex exposure may have fundamentally and qualitatively different physiological consequences for health in males and females.

Intestinal GPDH-1 regulates high glucose diet induced lifespan extension in aged worms.

A high glucose diet (HGD) is associated with many metabolic diseases including type 2 diabetes, and cardiovascular diseases. Additionally, a HGD increases the oxidative stress resistance of young animals but shortens their lifespan. To investigate the role of HGD feeding on the aging of aged animals, we tested for oxidative stress resistance and changes in lifespan using C. elegans. We showed that a HGD extends the lifespan of aged worms that are dependent on oxidative stress resistance. Furthermore, we measured the lifespan of oxidative stress responding genes of HGD-fed worms. We found that gpdh-1 and col-92 are highly expressed in HGD and paraquat (PQ) treated worms. Further experiments indicated that intestinal gpdh-1 is essential for the HGD induced lifespan extension of aged worms. Our studies provide new insights into understanding the correlation between glucose metabolism, oxidative stress resistance, and aging.

Effects of age on face perception: Reduced eye region discrimination ability but intact holistic processing.

While age-related decline in face recognition memory is well-established, the degree of decline in face perceptual abilities across the lifespan and the underlying mechanisms are incompletely characterized. In the present study, we used the part-whole task to examine lifespan changes in holistic and featural processing. After studying an intact face, participants are tested for memory of a face part (eyes, nose, mouth) with the target and foil part presented either in isolation or in the context of the whole face. To the extent that parts are encoded into a holistic face representation, an advantage is expected for part recognition when tested in the whole face condition. The task therefore provides measures of holistic processing (whole-over-isolated-part trial advantage) and featural processing for each part when tested in isolation. Using a large sample of 3,341 online participants aged 18-69 years, we found that while discrimination of the eye region decreased beginning in the 50s, both mouth discrimination accuracy and the holistic advantage of whole versus part trial discrimination were stable with age. In separate analyses by gender, we found that age-related declines in eye region accuracy were more pronounced in males than females. We discuss potential mechanistic explanations for this eye region-specific decline with age, including age-related hearing loss directing attention toward the mouth. Further, we discuss how this could be related to the age-related positivity effect, which is associated with reduced sensitivity to eye-related emotions (e.g., anger) but preserved mouth-related emotion sensitivity (e.g., happiness). (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Differential AMPK-mediated metabolic regulation observed in hibernation-style polymorphisms in Siberian chipmunks.

Hibernation is a unique physiological phenomenon allowing extreme hypothermia in endothermic mammals. Hypometabolism and hypothermia tolerance in hibernating animals have been investigated with particular interest; recently, studies of cultured cells and manipulation of the nervous system have made it possible to reproduce physiological states related to hypothermia induction. However, much remains unknown about the periodic regulation of hibernation. In particular, the physiological mechanisms facilitating the switch from an active state to a hibernation period, including behavioral changes and the acquisition of hypothermia tolerance remain to be elucidated. AMPK is a protein known to play a central role not only in feeding behavior but also in metabolic regulation in response to starvation. Our previous research has revealed that chipmunks activate AMPK in the brain during hibernation. However, whether AMPK is activated during winter in non-hibernating animals is unknown. Previous comparative studies between hibernating and non-hibernating animals have often been conducted between different species, consequently it has been impossible to account for the effects of phylogenetic differences. Our long-term monitoring of siberian chipmunks, has revealed intraspecific variation between those individuals that hibernate annually and those that never become hypothermic. Apparent differences were found between hibernating and non-hibernating types with seasonal changes in lifespan and blood HP levels. By comparing seasonal changes in AMPK activity between these polymorphisms, we clarified the relationship between hibernation and AMPK regulation. In hibernating types, phosphorylation of p-AMPK and p-ACC was enhanced throughout the brain during hibernation, indicating that AMPK-mediated metabolic regulation is activated. In non-hibernating types, AMPK and ACC were not seasonally activated. In addition, AMPK activation in the hypothalamus had already begun during high Tb before hibernation. Changes in AMPK activity in the brain during hibernation may be driven by circannual rhythms, suggesting a hibernation-regulatory mechanism involving AMPK activation independent of Tb. The differences in brain AMPK regulation between hibernators and non-hibernators revealed in this study were based on a single species thus did not involve phylogenetic differences, thereby supporting the importance of brain temperature-independent AMPK activation in regulating seasonal metabolism in hibernating animals.

In support of researching later-life language variation and change

Variationist sociolinguists must commit to developing age-comprehensive theories of sociolinguistic variation and lifespan change. They must extend analyses of patterns of language variation and change to include the oft-neglected later life-course, and must embrace cross-disciplinary knowledge exchange to identify and explore those ageing-associated biological, psychological and social changes that may impact language use in later life. Improved understanding of later-life linguistic diversity and instability will enhance current sociolinguistic theorizing and potentially also provide hypotheses about factors impacting language use in the early life-course. It will promote a richer understanding of the extent and interconnectedness of behaviour changes in later life. And it will also benefit the community of older adult language users by celebrating them as competent and agentive language users.

Lycium barbarum glycopetide prolong lifespan and alleviate Parkinson's disease in Caenorhabditis elegans.

Lycium barbarum glycopeptide (LbGp) is the main bioactive compound extracted from the traditional Chinese medicine. L. barbarum berries and has been proven to have numerous health benefits, including antioxidative, anti-inflammatory, anticancer, and cytoprotective activities. However, the antiaging effect of LbGp remains unknown. The lifespan and body movement of C. elegans were used to evaluate the effect of LbGp on lifespan and health span. The thrashing assay was used to determine the role of LbGp in Parkinson's disease. To investigate the mechanisms of LbGp-induced antiaging effects, we analyzed changes in lifespan, movement, and the expression of longevity-related genes in a series of worm mutants after LbGp treatment. We found that LbGp treatment prolonged the lifespan and health span of C. elegans. Mechanistically, we found that LbGp could activate the transcription factors DAF-16/FOXO, SKN-1/Nrf2, and HSF-1, as well as the nuclear receptor DAF-12, thereby upregulating longevity-related genes to achieve lifespan extension. In addition, we found that the lifespan extension induced by LbGp partially depends on mitochondrial function. Intriguingly, LbGp also ameliorated neurodegenerative diseases such as Parkinson's disease in a DAF-16-, SKN-1-, and HSF-1-dependent manner. Our work suggests that LbGp might be a viable candidate for the treatment and prevention of aging and age-related diseases.

Tracing the development and lifespan change of population-level structural asymmetry in the cerebral cortex.

Cortical asymmetry is a ubiquitous feature of brain organization that is subtly altered in some neurodevelopmental disorders, yet we lack knowledge of how its development proceeds across life in health. Achieving consensus on the precise cortical asymmetries in humans is necessary to uncover the developmental timing of asymmetry and the extent to which it arises through genetic and later influences in childhood. Here, we delineate population-level asymmetry in cortical thickness and surface area vertex-wise in seven datasets and chart asymmetry trajectories longitudinally across life (4-89 years; observations = 3937; 70% longitudinal). We find replicable asymmetry interrelationships, heritability maps, and test asymmetry associations in large-scale data. Cortical asymmetry was robust across datasets. Whereas areal asymmetry is predominantly stable across life, thickness asymmetry grows in childhood and peaks in early adulthood. Areal asymmetry is low-moderately heritable (max h2SNP ~19%) and correlates phenotypically and genetically in specific regions, indicating coordinated development of asymmetries partly through genes. In contrast, thickness asymmetry is globally interrelated across the cortex in a pattern suggesting highly left-lateralized individuals tend towards left-lateralization also in population-level right-asymmetric regions (and vice versa), and exhibits low or absent heritability. We find less areal asymmetry in the most consistently lateralized region in humans associates with subtly lower cognitive ability, and confirm small handedness and sex effects. Results suggest areal asymmetry is developmentally stable and arises early in life through genetic but mainly subject-specific stochastic effects, whereas childhood developmental growth shapes thickness asymmetry and may lead to directional variability of global thickness lateralization in the population.

Examining the potential for lead-time bias by estimating stage-specific proportions of deaths due to diagnosed cancer.

10535 Background: Lead-time bias occurs when cancer is detected earlier in time, but with no change in lifespan. Cause of death is not susceptible to lead-time bias; therefore, stratifying cause of death by cancer stage informs the potential for lead-time bias in early detection across cancer types. Methods: Using recent data from 17 US Surveillance, Epidemiology, and End Results (SEER) cancer registries for 1 152 610 first incident primary cancers among patients aged 50–84 years at diagnosis in 2006–2010, we evaluated proportional causes of death by cancer type and uniformly classified stage at diagnosis (American Joint Committee on Cancer, 6th edition), following or extrapolating all patients until death. Results: A minority of cancer patients diagnosed at stages I–II (27%) went on to die from their index cancer, whereas most stage IV cancer patients (85%) did. For patients diagnosed with stage I cancer at all sites combined, an estimated 26% of deaths were due to the index cancer, 61% due to non-cancer causes, and 12% due to a subsequent primary (non-index) cancer. At stage II, 27% of deaths were due to the index cancer, 60% due to non-cancer causes, and 13% due to a non-index cancer. In contrast, at stage IV, 85% of deaths were attributed to the index cancer, with 13% non-cancer and 2% non-index-cancer deaths. Index cancer mortality from stages I–II cancer was proportionally lowest for thyroid, melanoma, uterus, prostate, and breast, and highest for pancreas, liver, esophagus, lung, and stomach. Leading causes of non-index cancer death (lung, pancreas, and colorectal) and non-cancer death (heart disease and COPD) at each stage were similar to those in the general US population. Non-White racial/ethnic groups, including Hispanics and non-Hispanic Blacks, Asian Americans/Pacific Islanders, and American Indians/Alaska Natives, experienced a higher percentage of deaths from stages I–II cancer than non-Hispanic Whites. Conclusions: Across all cancer types, the percentage of patients who went on to die from their cancer was three times greater at stage IV than at stages I–II. As mortality patterns are not influenced by lead-time bias, these data suggest that earlier stage at diagnosis is broadly, if not uniformly, associated with substantially reduced risk of cause-specific death from cancer; therefore, early detection is likely to improve outcomes across cancer types, including those currently unscreened. [Table: see text]

Final step of B-cell differentiation into plasmablasts; the right time to activate plasma cell PIM2 kinase

The differentiation of B cells into antibody-secreting plasma cells is a complex process that involves extensive changes in morphology, lifespan, and cellular metabolism to support the high rates of antibody production. During the final stage of differentiation, B cells undergo significant expansion of their endoplasmic reticulum and mitochondria, which induces cellular stress and may lead to cell death in absence of effective inhibition of the apoptotic pathway. These changes are tightly regulated at transcriptional and epigenetic levels, as well as at post-translational level, with protein modifications playing a critical role in the process of cellular modification and adaptation.Our recent research has highlighted the pivotal role of the serine/threonine kinase PIM2 in B cell differentiation, from commitment stage to plasmablast and maintenance of expression in mature plasma cells. PIM2 has been shown to promote cell cycle progression during the final stage of differentiation and to inhibit Caspase 3 activation, raising the threshold for apoptosis. In this review, we examine the key molecular mechanisms controlled by PIM2 that contribute to plasma cell development and maintenance.

Early-life telomere length predicts life-history strategy and reproductive senescence in a threatened wild songbird.

Telomeres are well known for their associations with lifespan and ageing across diverse taxa. Early-life telomere length can be influenced by developmental conditions and has been shown positively affect lifetime reproductive success in a limited number of studies. Whether these effects are caused by a change in lifespan, reproductive rate or perhaps most importantly reproductive senescence is unclear. Using long-term data on female breeding success from a threatened songbird (the hihi, Notiomystis cincta), we show that the early-life telomere length of individuals predicts the presence and rate of future senescence of key reproductive traits: clutch size and hatching success. In contrast, senescence of fledging success is not associated with early-life telomere length, which may be due to the added influence of biparental care at this stage. Early-life telomere length does not predict lifespan or lifetime reproductive success in this species. Females may therefore change their reproductive allocation strategy depending on their early developmental conditions, which we hypothesise are reflected in their early-life telomere length. Our results offer new insights on the role that telomeres play in reproductive senescence and individual fitness and suggest telomere length can be used as a predictor for future life history in threatened species.

Community and lifespan changes in music: Sociophonetic variation in Laurentian French

Previous studies on English have highlighted various instances where individual singers or small groups change which dialectal features appear in their music (e.g. Trudgill 1997; Beal 2009; Coupland 2011; Eberhardt & Freeman 2015; Lyon 2019). Whereas corpus studies on music have the option between real-time or apparent-time analyses, most previous research on music has largely been conducted via case studies on change across a singer or group’s career (see Gibson in press a). Focusing on Laurentian French (also known as Quebec French or Canadian French), multiple singers may moderate dialectal traits in music due to their albums being released internationally, where the dialect faces stigma (Szlezák 2015). We further hypothesize that pop singers are especially sensitive to international norms and stigma because they are more likely to market abroad due to pop music’s greater international appeal (Grenier 1993). We examine non-lengthened high vowel laxing in closed final syllables (e.g. /vit/ [vɪt] vite ‘fast’; Dumas 1983), a process characteristic of Laurentian French that is categorical (Côté 2012) and nonstigmatized (Lappin 1982; Paradis & Dolbec 1998; Reinke et al. 2006) within the dialect. We expand the study of dialectal traits in music beyond English by using a new corpus of 20 Québécois singers who sing in French and are of the Laurentian French dialect. Additionally, we analyze the patterning of groups of singers across their careers, rather than the patterning of a single singer, and analyze real-time change of groups as opposed to individuals

Drosophila Models Reveal Properties of Mutant Lamins That Give Rise to Distinct Diseases.

Mutations in the LMNA gene cause a collection of diseases known as laminopathies, including muscular dystrophies, lipodystrophies, and early-onset aging syndromes. The LMNA gene encodes A-type lamins, lamins A/C, intermediate filaments that form a meshwork underlying the inner nuclear membrane. Lamins have a conserved domain structure consisting of a head, coiled-coil rod, and C-terminal tail domain possessing an Ig-like fold. This study identified differences between two mutant lamins that cause distinct clinical diseases. One of the LMNA mutations encodes lamin A/C p.R527P and the other codes lamin A/C p.R482W, which are typically associated with muscular dystrophy and lipodystrophy, respectively. To determine how these mutations differentially affect muscle, we generated the equivalent mutations in the Drosophila Lamin C (LamC) gene, an orthologue of human LMNA. The muscle-specific expression of the R527P equivalent showed cytoplasmic aggregation of LamC, a reduced larval muscle size, decreased larval motility, and cardiac defects resulting in a reduced adult lifespan. By contrast, the muscle-specific expression of the R482W equivalent caused an abnormal nuclear shape without a change in larval muscle size, larval motility, and adult lifespan compared to controls. Collectively, these studies identified fundamental differences in the properties of mutant lamins that cause clinically distinct phenotypes, providing insights into disease mechanisms.