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Survival models which incorporate frailties are common in time-to-event data collected over distinct spatial regions. While incomplete data are unavoidable and a common complication in statistical analysis of spatial survival research, most researchers still ignore the missing data problem. In this paper, we propose a geostatistical modeling approach for incomplete spatially correlated survival data. We achieve this by exploring missingness in outcome, covariates, and spatial locations. In the process, we analyze incomplete spatially-referenced survival data using a Weibull model for the baseline hazard function and correlated log-Gaussian frailties to model spatial correlation. We illustrate the proposed method with simulated data and an application to geo-referenced COVID-19 data from Ghana. There are several disagreements between parameter estimates and credible intervals widths obtained using our proposed approach and complete case analysis. Based on these findings, we argue that our approach provides more reliable parameter estimates and has higher predictive accuracy. [ABSTRACT FROM AUTHOR]

Abstract: In a society experiencing an accelerating increase in the middle- and old-age population, there is an urgent need to address age-dependent frailties by a paradigm shift, i.e. a new medical strategy to combat middle-age decline at the stage before incipient old-age problems develop into full-blown diseases. We suggest that a decline in cellular health status occurs at mid-life, and that this decline may involve a universal or system-specific programmatic shift of signaling control. This decline, although sub-clinical and asymptomatic, may precipitate increased risk of late-life diseases. The putative control for this mid-life cellular decline may be governed by a recently discovered group of molecular species, the microRNAs, small RNAs of ∼22 nucleotide bases. In general microRNAs, while themselves not coding for any protein product, negatively regulate the expression of target genes by either degrading their message or inhibiting translation by binding to their 3′-untranslated region (UTR). Thus, possible derailment of these negative regulators for gene expression in mid-life may be the putative force inducing molecular frailty in individual cell signaling, and in time leading to tissue-wide dysfunction. A challenge for future research is then to identify these dysfunctional microRNAs, in order to develop advance diagnosis and therapy to combat mid-life decline, a preventive medicine approach to block, delay or reduce the risk of old-age diseases. [Copyright &y& Elsevier]