About

Christina Finch currently serves as the Deputy Director of the Response Geospatial Office at the Federal Emergency Management Agency (FEMA). The RGO specializes in providing geospatial information that allows decision makers to prepare for, protect against, respond to, recover from, and mitigate all hazards. Christina previously managed the National Hurricane Program (NHP) at FEMA. She has more than fifteen years of experience in emergency management and has worked across the disaster life cycle (preparedness, mitigation, response, and recovery) to inform data-driven decisions. Christina has specific expertise in hurricane planning, evacuation modeling, mitigation, disaster operations, geospatial technology, socioeconomic vulnerability, risk communication, and community resilience. Christina earned an MS in geography from the University of South Carolina, and her academic research focused on the development of a composite metric of social vulnerability to identify spatial disparities in the ability to prepare, respond, cope, and recover from environmental hazards and disasters. Christina is passionate about addressing the gap between emergency management research and practice and developing the next generation of emergency managers.

Research topics

• Medicine
• Internal medicine
• Biology
• Immunology
• Chemistry
• Endocrinology
• Pathology
• Genetics
• Machine Learning
• Pharmacology
• Computer Science
• Environmental health
• Biophysics
• Environmental chemistry
• Ecology
• Radiology
• Anatomy
• Computational biology
• Gerontology
• Psychiatry
• Psychology
• Toxicology

Selected publications

• Socio-economic influences from egg to exit: Emerging biology

  Ageing Research Reviews · 2026-03-20

  articleOpen accessSenior author

  Socio-economic status (SES) impacts life-long health from early development to old age. We review SES differences in biological factors that begin before fertilization and extend into later life, 'egg to exit'. SES gradients are shown in onset and prevalence of chronic conditions including cardiovascular disease, diabetes and dementia, leading up to a 15-year difference in life expectancy in some countries. Our analysis is limited to high-income countries and does not include detailed discussion of gender or ethnic differences. We develop a comprehensive multi-disciplinary framework for SES gradients in health and aging extending from the population level to gene expression. This framework integrates biological processes such as developmental programming and epigenetic regulation into a unified life-course model. Key components in the ´SES exposome´ are diet, cigarette smoke, environmental and household air pollution, and psychosocial stress. Interactions between psychosocial stress, diet and environmental pollution are incompletely understood. Inflammation and oxidative damage occur in in many organs. Some mechanisms are experimentally testable in cells and rodents, but these models cannot evaluate human aging for psychosocial factors and multi-generational interactions. SES influences are modified by social mobility ('SES fluidity'), yet some biological changes, such as DNA mutations and collagen cross-linking, have limited reversibility. This integrative analysis provides a framework for future research and potential remediation of SES constraints on health and aging.

  PublisherDOI

• High Prevalence of Cerebrovascular Calcifications and Clinical Correlates in Indigenous Bolivian Forager‐Horticulturalists: A Population‐Based Observational Study

  Journal of the American Heart Association · 2026-01-30

  articleOpen access

  BACKGROUND: Intracranial arteriosclerosis (large- and small-vessel disease) is considered a risk factor for major neurological disorders, such as stroke, cognitive impairment, and dementia. While most studies investigating intracranial arteriosclerosis include individuals from industrialized populations, the prevalence and clinical meaning of intracranial vascular calcifications in populations with a subsistence lifestyle is unknown. METHODS: In this population-based study evaluating data collected between 2017 and 2019 from Tsimane and Moseten people, 2 indigenous populations of forager-horticulturalists living in the Bolivian Amazon, we used computed tomography to determine the prevalence of vascular calcifications in the intracranial internal carotid arteries, vertebral arteries, and lenticulostriate arteries within the basal ganglia, and their association with demographic characteristics, brain atrophy, cognitive performance, and clinical factors. RESULTS: Our analysis included 1232 individuals who underwent a head computed tomography scan. Intracranial vascular calcifications were found in most individuals (>90%) and their prevalence was higher than that reported for age-equivalent industrialized populations. These calcifications were significantly associated with higher age, brain atrophy, worse cognitive performance, and parkinsonian symptoms. CONCLUSIONS: Despite the physically active subsistence lifestyle and the low rates of typical cardiovascular risk factors and coronary artery disease, intracranial vascular calcifications are common in these Bolivian Amerindian people, suggesting that alternative factors may contribute to intracranial arteriosclerosis and a novel dementia phenotype.

  PublisherDOI

• Induction of ferroptotic and amyloidogenic signatures linked to Alzheimer’s disease by chemically distinct air pollutants

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-07 · 1 citations

  articleOpen access

  ABSTRACT Air pollution (AirP) exposure is associated with increased Alzheimer’s disease (AD) risk, yet AirP is chemically heterogeneous, complicating identification of shared pathogenic drivers. We examined acute cortical responses to two metal-rich AirP sources, diesel exhaust particles (DEP) and World Trade Center (WTC) dust, and compared them to woodsmoke (WS), a particulate exposure with low metal content. DEP and WTC elicited highly convergent transcriptional responses, sharing over 1200 differentially expressed genes linked to inflammation, ferroptosis, neuronal remodeling, and amyloid processing. These changes were accompanied by impaired antioxidant activity and increased lipid peroxidation within lipid rafts, a membrane microdomain critical for amyloid processing, resulting in increased Aβ generation. In contrast, WS produced a distinct transcriptional signature and failed to induce ferroptotic priming or lipid peroxidation, consistent with its low metal composition. Together, these findings implicate metals as a shared driver linking diverse AirP exposures to amyloidogenic vulnerability and elevated AD risk. Graphical Abstract Acute AirP exposure converges on ferroptotic priming, amyloidogenic processing, and white-matter vulnerability. Acute exposure to metal-rich AirP, such as DEP or WTC introduces redox-active metals and particulate matter that promote lipid peroxidation, amyloidogenesis, and altered transcriptional regulation in the brain. AirP exposure engages xenobiotic metabolism pathways (AhR/ARNT), activates iron and heme handling through ferritinophagy (NCOA4) and heme oxygenase activity (HMOX1), and blunts lipid peroxide detoxification systems, including glutathione peroxidase 4 (GPx4), ferroptosis suppressor protein 1 (FSP1), and glutathione (GSH) synthesis. These changes promote ferroptotic priming and lipid raft oxidation, facilitating amyloid precursor protein (APP) processing by secretases (ADAM10, BACE1, γ-secretase) and increasing amyloid-β (Aβ) generation. In parallel, transcriptional and cell-state remodeling involving neuronal and oligodendrocyte responses contribute to selective white-matter vulnerability, particularly within the corpus callosum. Together, these pathways provide a mechanistic framework linking acute AirP exposure to convergent oxidative, amyloidogenic, and microstructural changes relevant to Alzheimer’s disease pathology.

  PublisherDOI

• Acute air pollution exposure downregulates ferroptosis protection genes causing increases in amyloid peptides and lipid peroxidation

  Free Radical Biology and Medicine · 2025-10-30

  article
  PublisherDOI

• Author response for "Inflammaging is minimal among forager-horticulturalists in the Bolivian Amazon"

  2025-04-28

  peer-review
  PublisherDOI

• Inflammaging is minimal among forager-horticulturalists in the Bolivian Amazon

  Proceedings of the Royal Society B Biological Sciences · 2025-08-01 · 2 citations

  article

  An increase in chronic systemic inflammation in later life, termed inflammaging, is implicated in health risk. However, it is unclear whether inflammaging develops in all human populations, or if it is the product of environmental mismatch. We assessed inflammaging in Tsimane forager-horticulturalists of the Bolivian Amazon, using serum cytokines in a primarily cross-sectional sample (1134 samples from n = 714 individuals, age 39–94, 51.3% female). IL-6 was positively associated with age ( β = 0.013, p < 0.01). However, other pro-inflammatory markers, including IL-1β and TNF-α, did not increase with age ( β = −0.005 and β = −0.001, respectively). We then compared the Moseten, a neighbouring population that has experienced greater market integration (423 samples from n = 380 individuals, age 39–85, 48.2% female). The Moseten also showed a positive age association for IL-6 that attenuated at later ages (age β = 0.025, p < 0.01; age 2 β = −0.001, p < 0.05). Further, IL-1β and TNF-α were both positively associated with age ( β = 0.021, p < 0.05 and β = 0.011, p < 0.01, respectively). Our results demonstrate minimal inflammaging in the Tsimane, highlighting variation across populations in this age-related process. They also suggest that inflammaging is exacerbated by lifestyle shifts.

  PublisherDOI

• Physical activity mediates age differences in cognition among Tsimane forager-horticulturalists

  The Journals of Gerontology Series A · 2025-07-23

  articleOpen access

  BACKGROUND: The Tsimane and Moseten of the Bolivian Amazon are highly physically active and exhibit low rates of cognitive impairment and brain atrophy. METHODS: We use structural equation modelling to examine how their physical activity levels mediate the relationship between (1) age and cognition, and (2) age and cognition via brain volume (BV). RESULTS: Tsimane males (n = 305, mean ± SD age = 59.94 ± 9.68) and Tsimane females (n = 265, mean ± SD age = 59.28 ± 9.79) exhibit significantly higher levels of physical activity than Moseten males (n = 106, mean ± SD age = 58.15 ± 9.93) and Moseten females (n = 96, mean ± SD age = 56.63 ± 9.69). Physical activity significantly mediates the relationship between age and cognition in Tsimane males (indirect effect estimate ݼ = -0.01, P < .01) and Tsimane females (indirect effect estimate ݼ = -0.04, P = .01), but not in Moseten males or females. CONCLUSIONS: Among Tsimane males, who are more physically active than Tsimane females, the association between age and cognition via BV is significantly mediated by physical activity. Among Tsimane females, mediation occurs directly via physical activity, bypassing BV. These results suggest that mechanisms of cognitive differences across ages differ by sex and population. Studying the relationship between brain atrophy and lifestyle in nonindustrialized populations elucidates biological and environmental correlates of brain health.

  PublisherOA PDFDOI

• Abstract Tu0086: Gene-Environment Interaction Between the <i>TRIP4</i> Locus and Air Pollution Exposure Increases Risk of Coronary Artery Disease

  Arteriosclerosis Thrombosis and Vascular Biology · 2025-04-01

  article

  Introduction: Coronary artery disease (CAD) has a strong genetic component but known susceptibility loci only explain a fraction of its overall heritability. This observation suggests that other factors, such as gene-environment (GxE) interactions, can also contribute to CAD risk. In this regard, particulate matter &lt;2.5mM in diameter (PM 2.5 ) is one environmental pollutant that has consistently been associated with CAD. However, very few interactions between PM 2.5 exposure and genetic determinants of CAD have been identified. Hypothesis: We tested the hypothesis that risk of CAD could be mediated through GxE interactions between known susceptibility variants and PM 2.5 levels. Methods: Logistic regression was used to test 320 CAD loci for GxE interactions with PM 2.5 in the GeneBank and UK Biobank cohorts (total n=381,867). Expression quantitative trait locus (eQTL) data, in vitro transcriptomics profiling of human endothelial cells exposed to diesel exhaust or diesel exhaust particles (DEP) extract, and in vivo gene expression analyses of aortas from mice exposed to DEP or filtered air were used to prioritize positional candidate genes. Results: In the UK Biobank, CAD risk increased with a 2SD rise in PM 2.5 (OR=1.11, 95% CI 1.08-1.14; P=8.2x10 -13 ), NO 2 (OR=1.06, 95% CI 1.03-1.09; P=6.8x10 -5 ), and NO x (OR=1.07, 95% CI 1.04-1.10; P=7.4x10 -7 ). A GxE interaction was identified with a variant (rs6494488; A&gt;G) on chromosome 15 (P-int=1.2x10 -4 ). PM 2.5 exposure increased CAD risk more in AA homozygotes (OR=1.28, 95% CI 1.25-1.32; P=8.4x10 -60 ) than in AG heterozygotes (OR=1.17, 95% CI 1.11-1.23; P=1.4x10 -9 ) but not in GG homozygotes (OR=1.06, 95% CI 0.92-1.22; P=0.42). Of the genes at this locus, the A allele was only associated with lower TRIP4 mRNA in cardiometabolic tissues, with TRIP4 ~11% lower in CAD aortas than controls (P=2.7x10 -4 ). Human endothelial cells exposed to diesel exhaust or DEP extract in data sets showed reduced TRIP4 expression (P=2.8x10 -4 and P=0.02, respectively). Long-term exposure of mice to DEP decreased mRNA levels of Trip4 (P=5.9x10 -3 ) in the aorta but not any other positional candidate gene at the chromosome 15 locus. Conclusions: These results support the concept that risk of CAD can be influenced through interactions between genetic factors and air pollution exposure and suggest that one such GxE interaction at a chromosome 15 locus is potentially mediated by the athero-protective properties of TRIP4 at the level of the vessel wall.

  PublisherDOI

• Down syndrome with Alzheimer's disease brains have increased iron and associated lipid peroxidation consistent with ferroptosis

  Alzheimer s & Dementia · 2025-06-01 · 6 citations

  articleOpen accessSenior author

  INTRODUCTION: Cerebral microbleeds (MBs) are associated with sporadic Alzheimer's disease (AD) and Down syndrome with AD (DSAD). Higher MB iron may cause iron-mediated lipid peroxidation. We hypothesize that amyloid deposition is linked to MB iron and that amyloid precursor protein (APP) triplication increases iron load and lipid peroxidation. METHODS: Prefrontal cortex and cerebellum of cognitively normal control (CTL), AD, and DSAD ApoE3,3 carriers were examined for proteins that mediated iron metabolism, antioxidant response, and amyloid processing in lipid rafts. RESULTS: Iron was twofold higher in DSAD than in CTL and AD. Iron storage proteins and lipid peroxidation were increased in the prefrontal cortex. The glutathione synthesis protein GCLM was decreased by 50% in both AD and DSAD. Activity of lipid raft GPx4, responsible for membrane repair, was decreased by at least 30% in AD and DSAD. DISCUSSION: DSAD shows greater lipid peroxidation than AD, consistent with greater MBs and iron load. HIGHLIGHTS: DSAD has increased ferroptotic-related changes compared to sporadic AD. Lipid rafts that process APP have a loss of protective antioxidant enzymes. Partial and mosaic trisomy lowers the amyloid and iron burden.

  PublisherOA PDFDOI

• Increase of brain Aβ peptides and secretase activity during normal aging in rodent and human

  GeroScience · 2025-10-14 · 1 citations

  articleOpen accessSenior authorCorresponding

  Age increases of brain amyloid plaques may be mediated by prior increase of soluble Aβ42. Here, we show that frontal cortex samples from brains of cognitively normal aging humans had progressively increased levels of soluble amyloid peptide Aβ40 throughout the lifespan. Aggregated amyloid fraction was subsequently obtained by formic acid, where Aβ42 showed increases only in humans over 90 years old when compared to those younger than 50. Similarly, aging wild-type mice without amyloid plaques had increases of both soluble Aβ40 and Aβ42, as previously shown in normal aging rats. Aging also alters secretase enzymes and processing of amyloid precursor protein (APP). Here, we isolate membrane domains known as lipid rafts, a site of APP cleavage. We found that lipid rafts isolated from mouse and human cerebral cortex showed age increases of β-secretase enzyme activity, while amyloidogenic secretase proteins levels BACE1 and PS1 decreased with age in mouse. Lipid rafts merit further study in aging and neurodegeneration.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01AG013499

  NIH · $4.5M · 2009

• Administrative Core

  NIH · $18.5M · 2018–2023

• Perimenopause in Brain Aging and Alzheimer's Disease

  NIH · $85.8M · 2006–2027

• NIH Grant R21AG050201

  NIH · $206k · 2019

• NIH Grant T32AG000093

  NIH · $7.2M · 2009

Frequent coauthors

• Todd E. Morgan

  Human Longevity (United States)

  137 shared

• Constantinos Sioutas

  University of Southern California

  64 shared

• Gregory S. Thomas

  University of California, Irvine

  61 shared

• Randall C. Thompson

  University of Missouri–Kansas City

  51 shared

• J. Kenneth Baillie

  Roslin Institute

  50 shared

• Bruno Fröhlich

  38 shared

• Irina Rozovsky

  University of Southern California

  37 shared

• Michael Gurven

  35 shared

Education

• PhD

  Rockefeller University

  1969