Cell wall integrity modulates HOOKLESS1 and PHYTOCHROME INTERACTING FACTOR4 expression controlling apical hook formation.

Formation of the apical hook in etiolated dicot seedlings results from differential growth in the hypocotyl apex and is tightly controlled by environmental cues and hormones, among which auxin and gibberellins (GAs) play an important role. Cell expansion is tightly regulated by the cell wall, but whether and how feedback from this structure contributes to hook development is still unclear. Here, we show that etiolated seedlings of the Arabidopsis (Arabidopsis thaliana) quasimodo2-1 (qua2) mutant, defective in pectin biosynthesis, display severe defects in apical hook formation and maintenance, accompanied by loss of asymmetric auxin maxima and of differential cell expansion. Moreover, qua2 seedlings show reduced expression of HOOKLESS 1 (HLS1) and PHYTOCHROME INTERACTING FACTOR 4 (PIF4), which are positive regulators of hook formation. Treatment of wild-type seedlings with the cellulose inhibitor isoxaben (isx) also prevents hook development and represses HLS1 and PIF4 expression. Exogenous GAs, loss of DELLA proteins or HLS1 overexpression partially restore hook development in qua2 and isx-treated seedlings. Interestingly, increased agar concentration in the medium restores, both in qua2 and isx-treated seedlings, hook formation, asymmetric auxin maxima and PIF4 and HLS1 expression. Analysis of plants expressing a FRET-based GA sensor indicate that isx reduces accumulation of GAs in the apical hook region in a turgor-dependent manner. Lack of the cell wall integrity sensor THESEUS 1, which modulates turgor loss point, restores hook formation in qua2 and isx-treated seedlings. We propose that turgor-dependent signals link changes in cell wall integrity to the PIF4-HLS1 signalling module to control differential cell elongation during hook formation.

Social and Environmental Characteristics Associated With Older Drivers' Use of Non-driving Transportation Modes.

Objective: We examined associations between older drivers' social and environmental characteristics and odds of using non-driving transportation modes. Methods: Using 2015 National Health and Aging Trends Study data for community-dwelling drivers (n = 5102), we estimated logistic regression models of associations between social characteristics, environmental characteristics, and odds of using non-driving transportation modes three years later. Results: Drivers had 20% increase in odds of getting rides three years later for each additional confidante (adjusted odds ratio [aOR] = 1.20, 95% confidence interval [CI]: 1.11-1.30). Drivers living in more walkable neighborhoods were more likely to walk to get places (National Walkability Index [NWI] score of 18 vs. 2 aOR = 1.71, 95% CI: 1.02-2.90) and take public transit three years later (NWI 18 vs. 2 aOR = 7.47, 95% CI: 1.69-33.0). Discussion: Identifying modifiable social and environmental characteristics can inform future interventions supporting older adults' health during the transition to non-driving.

Isolated unilateral alar ligamentous injury: illustrative cases.

BACKGROUND: Isolated unilateral alar ligament injury (IUALI) is a rare and likely underreported occurrence after upper cervical trauma, with only 16 cases documented in the literature to date. Patients generally present with neck pain, and definitive diagnosis is typically made by magnetic resonance imaging (MRI). Unfortunately, likely due in part to its rarity, there are no formal guidelines for the treatment of an IUALI. Furthermore, there is a limited understanding of the long-term consequences associated with its inadequate treatment. OBSERVATIONS: Here, the authors report on three pediatric patients, each found to have an IUALI after significant trauma. All patients presented with neck tenderness, and two of the three had associated pain-limited range of neck motion. Imaging revealed either a laterally deviated odontoid process on cervical radiographs and/or MRI evidence of ligamentous strain or discontinuity. Each patient was placed in a hard cervical collar for 1 to 2 months with excellent resolution of symptoms. A comprehensive review of the literature showed that all patients with IUALI who had undergone external immobilization with either rigid cervical collar or halo fixation had favorable outcomes at follow-up. LESSONS: For patients with IUALI, a moderate course of nonsurgical management with rigid external immobilization appears to be an adequate first-line treatment.

Getting Rides From Others As a Coping Mechanism in the Transition to Non-Driving.

OBJECTIVES: To characterize the effect of the actual and potential ability to get rides from others on older adults' driving reduction at 3-year follow-up in the United States. METHODS: We analyzed National Health and Aging Trends Study data from community-dwelling drivers in 2015 (unweighted n = 5,102). We used weighted logistic regression models to estimate whether getting rides from others in 2015 was associated with older adults increasing the number of driving behaviors they avoided, decreasing the frequency with which they drove, or not driving at 3-year follow-up after adjusting for biopsychosocial variables. We also measured presence of social network members living nearby including household and non-household members and estimated associated odds of driving reduction at 3-year follow-up. RESULTS: Older adults who got rides from others in 2015 had greater odds of reporting no longer driving at 3-year follow-up compared to those who did not get rides (adjusted odds ratio [aOR] = 1.53, 95% confidence interval [CI]: 1.11-2.11). We found no statistically significant association between older adults living with others or having more nearby confidantes outside their household and their odds of reducing driving at 3-year follow-up. DISCUSSION: These findings suggest that getting rides from others plays an important role in the transition to non-driving for older adults. Future research should examine whether other aspects of social networks (e.g., type, quality, and closer proximity) might also be key modifiable coping factors for older adults transitioning to non-driving.

Measuring Age-Friendliness of Transportation and Mobility Characteristics in Communities: A Scoping Review.

BACKGROUND AND OBJECTIVES: Age-friendly communities are those with characteristics that can support and promote healthy aging. Among the common domains of these characteristics, transportation and neighborhood spaces are particularly relevant for older adults maintaining mobility in their communities. The objective of this scoping review is to provide a synthesis of age-friendly community indicators, developed for research and planning, that evaluate characteristics most associated with community-level mobility, specifically transportation and neighborhood spaces. RESEARCH DESIGN AND METHODS: We conducted a systematic search of PubMed, Scopus, Medline, APA PsychInfo, CINAHL Plus, SocIndex, Academic Search Premier, and Web of Science. We reviewed 8 articles and reports that described the development or evaluation of a set of generalizable indicators to measure the age-friendliness of a community's transportation and neighborhood spaces resources. RESULTS: Indicators of transportation and neighborhood spaces ranged from self-reported measures of accessibility and convenience to objective measures of the availability and cost of services. Explicit discussion of mobility at the community level was variable in these records, and few authors specifically discussed common life transitions impacted by these age-friendly community indicators, such as driving cessation. DISCUSSION AND IMPLICATIONS: Although age-friendly communities are a well-established goal for promoting healthy aging, our review found few validated approaches for measuring age-friendliness that researchers and communities can use to investigate mobility at the community level. This is an important gap in studying life transitions such as driving cessation. Further research can provide a better understanding of which community characteristics support ongoing mobility.

Does Subsidized Housing Prevent Health Decline and 2-Year Mortality Among Low-Income Older Renters?

BACKGROUND AND OBJECTIVES: A growing number of older adults in the United States need subsidized housing, but only 36% of eligible households receive assistance. The purpose of this study is to examine if older renters living in subsidized housing are less likely to experience health decline and mortality over 2 years compared to low-income older renters who are likely eligible, but do not receive assistance. RESEARCH DESIGN AND METHODS: Baseline data include 671 subsidized and unsubsidized low-income older renters from the 2015 National Health and Aging Trends Study. Outcomes of interest include self-rated health decline, developing a new activity limitation, or 2-year mortality between 2015 and 2017. Weighted stepwise logistic regression models test (a) if subsidized older renters were less likely to experience health decline or 2-year mortality compared to unsubsidized older renters, and (b) if housing quality and neighborhood factors mediate the association between subsidized housing and health decline/mortality. RESULTS: Subsidized older renters were less likely to develop a new activity limitation compared to unsubsidized older renters, but there was not a statistically significant difference in experiencing self-rated health decline or 2-year mortality by subsidized housing status. Housing quality and neighborhood factors did not significantly mediate this association. DISCUSSION AND IMPLICATIONS: The results provide some support that improving access to subsidized housing for low-income older renters may have additional health benefits, even in the short term. To inform program improvements and maximize potential health benefits, more research is needed to understand the specific health-promoting features of subsidized housing.

Contribution of Somatic Ras/Raf/Mitogen-Activated Protein Kinase Variants in the Hippocampus in Drug-Resistant Mesial Temporal Lobe Epilepsy.

Importance: Mesial temporal lobe epilepsy (MTLE) is the most common focal epilepsy subtype and is often refractory to antiseizure medications. While most patients with MTLE do not have pathogenic germline genetic variants, the contribution of postzygotic (ie, somatic) variants in the brain is unknown. Objective: To test the association between pathogenic somatic variants in the hippocampus and MTLE. Design, Setting, and Participants: This case-control genetic association study analyzed the DNA derived from hippocampal tissue of neurosurgically treated patients with MTLE and age-matched and sex-matched neurotypical controls. Participants treated at level 4 epilepsy centers were enrolled from 1988 through 2019, and clinical data were collected retrospectively. Whole-exome and gene-panel sequencing (each genomic region sequenced more than 500 times on average) were used to identify candidate pathogenic somatic variants. A subset of novel variants was functionally evaluated using cellular and molecular assays. Patients with nonlesional and lesional (mesial temporal sclerosis, focal cortical dysplasia, and low-grade epilepsy-associated tumors) drug-resistant MTLE who underwent anterior medial temporal lobectomy were eligible. All patients with available frozen tissue and appropriate consents were included. Control brain tissue was obtained from neurotypical donors at brain banks. Data were analyzed from June 2020 to August 2022. Exposures: Drug-resistant MTLE. Main Outcomes and Measures: Presence and abundance of pathogenic somatic variants in the hippocampus vs the unaffected temporal neocortex. Results: Of 105 included patients with MTLE, 53 (50.5%) were female, and the median (IQR) age was 32 (26-44) years; of 30 neurotypical controls, 11 (36.7%) were female, and the median (IQR) age was 37 (18-53) years. Eleven pathogenic somatic variants enriched in the hippocampus relative to the unaffected temporal neocortex (median [IQR] variant allele frequency, 1.92 [1.5-2.7] vs 0.3 [0-0.9]; P = .01) were detected in patients with MTLE but not in controls. Ten of these variants were in PTPN11, SOS1, KRAS, BRAF, and NF1, all predicted to constitutively activate Ras/Raf/mitogen-activated protein kinase (MAPK) signaling. Immunohistochemical studies of variant-positive hippocampal tissue demonstrated increased Erk1/2 phosphorylation, indicative of Ras/Raf/MAPK activation, predominantly in glial cells. Molecular assays showed abnormal liquid-liquid phase separation for the PTPN11 variants as a possible dominant gain-of-function mechanism. Conclusions and Relevance: Hippocampal somatic variants, particularly those activating Ras/Raf/MAPK signaling, may contribute to the pathogenesis of sporadic, drug-resistant MTLE. These findings may provide a novel genetic mechanism and highlight new therapeutic targets for this common indication for epilepsy surgery.

Auxin as an architect of the pectin matrix.

Auxin is a versatile plant growth regulator that triggers multiple signalling pathways at different spatial and temporal resolutions. A plant cell is surrounded by the cell wall, a complex and dynamic network of polysaccharides. The cell wall needs to be rigid to provide mechanical support and protection and highly flexible to allow cell growth and shape acquisition. The modification of the pectin components, among other processes, is a mechanism by which auxin activity alters the mechanical properties of the cell wall. Auxin signalling precisely controls the transcriptional output of several genes encoding pectin remodelling enzymes, their local activity, pectin deposition, and modulation in different developmental contexts. This review examines the mechanism of auxin activity in regulating pectin chemistry at organ, cellular, and subcellular levels across diverse plant species. Moreover, we ask questions that remain to be addressed to fully understand the interplay between auxin and pectin in plant growth and development.

Surgical strategies for intracranial meningioma in the molecular era.

INTRODUCTION: Surgical resection has long been the treatment of choice for meningiomas and is considered curative in many cases. Indeed, the extent of resection (EOR) remains a significant factor in determining disease recurrence and outcome optimization for patients undergoing surgery. Although the Simpson Grading Scale continues to be widely accepted as the measure of EOR and is used to predict symptomatic recurrence, its utility is under increasing scrutiny. The influence of surgery in the definitive management of meningioma is being re-appraised considering the rapid evolution of our understanding of the biology of meningioma. DISCUSSION: Although historically considered "benign" lesions, meningioma natural history can vary greatly, behaving with unexpectedly high recurrence rates and growth which do not always behave in accordance with their WHO grade. Histologically confirmed WHO grade 1 tumors may demonstrate unexpected recurrence, malignant transformation, and aggressive behavior, underscoring the molecular complexity and heterogeneity. CONCLUSION: As our understanding of the clinical predictive power of genomic and epigenomic factors matures, we here discuss the importance of surgical decision-making paradigms in the context of our rapidly evolving understanding of these molecular features.

Management of dynamic cervical kyphosis with dorsal epidural lipomatosis: a Hirayama disease variant? Illustrative case.

BACKGROUND: Hirayama disease, a cervical myelopathy characterized most commonly by a self-limiting atrophic weakness of the upper extremities, is a rare entity, scarcely reported in the literature. Diagnosis is made by spinal magnetic resonance imaging (MRI), which typically shows loss of normal cervical lordosis, anterior displacement of the cord during flexion, and a large epidural cervical fat pad. Treatment options include observation or cervical immobilization by collar or surgical decompression and fusion. OBSERVATIONS: Here, the authors report an unusual case of a Hirayama-like disease in a young White male athlete who presented with rapidly progressive paresthesia in all 4 extremities and no weakness. Imaging showed characteristic findings of Hirayama disease as well as worsened cervical kyphosis and spinal cord compression in cervical neck extension, which has not previously been reported. Two-level anterior cervical discectomy and fusion and posterior spinal fusion improved both cervical kyphosis on extension and symptoms. LESSONS: Given the disease's self-limiting nature, and a lack of current reporting, there remains no consensus on how to manage these patients. Such findings presented here demonstrate the potentially heterogeneous MRI findings that can be observed in Hirayama disease and emphasize the utility of aggressive surgical management in young, active patients whereby a cervical collar may not be tolerated.

The choroid plexus links innate immunity to CSF dysregulation in hydrocephalus.

The choroid plexus (ChP) is the blood-cerebrospinal fluid (CSF) barrier and the primary source of CSF. Acquired hydrocephalus, caused by brain infection or hemorrhage, lacks drug treatments due to obscure pathobiology. Our integrated, multi-omic investigation of post-infectious hydrocephalus (PIH) and post-hemorrhagic hydrocephalus (PHH) models revealed that lipopolysaccharide and blood breakdown products trigger highly similar TLR4-dependent immune responses at the ChP-CSF interface. The resulting CSF "cytokine storm", elicited from peripherally derived and border-associated ChP macrophages, causes increased CSF production from ChP epithelial cells via phospho-activation of the TNF-receptor-associated kinase SPAK, which serves as a regulatory scaffold of a multi-ion transporter protein complex. Genetic or pharmacological immunomodulation prevents PIH and PHH by antagonizing SPAK-dependent CSF hypersecretion. These results reveal the ChP as a dynamic, cellularly heterogeneous tissue with highly regulated immune-secretory capacity, expand our understanding of ChP immune-epithelial cell cross talk, and reframe PIH and PHH as related neuroimmune disorders vulnerable to small molecule pharmacotherapy.

A neural stem cell paradigm of pediatric hydrocephalus.

Pediatric hydrocephalus, the leading reason for brain surgery in children, is characterized by enlargement of the cerebral ventricles classically attributed to cerebrospinal fluid (CSF) overaccumulation. Neurosurgical shunting to reduce CSF volume is the default treatment that intends to reinstate normal CSF homeostasis, yet neurodevelopmental disability often persists in hydrocephalic children despite optimal surgical management. Here, we discuss recent human genetic and animal model studies that are shifting the view of pediatric hydrocephalus from an impaired fluid plumbing model to a new paradigm of dysregulated neural stem cell (NSC) fate. NSCs are neuroprogenitor cells that comprise the germinal neuroepithelium lining the prenatal brain ventricles. We propose that heterogenous defects in the development of these cells converge to disrupt cerebrocortical morphogenesis, leading to abnormal brain-CSF biomechanical interactions that facilitate passive pooling of CSF and secondary ventricular distention. A significant subset of pediatric hydrocephalus may thus in fact be due to a developmental brain malformation leading to secondary enlargement of the ventricles rather than a primary defect of CSF circulation. If hydrocephalus is indeed a neuroradiographic presentation of an inborn brain defect, it suggests the need to focus on optimizing neurodevelopment, rather than CSF diversion, as the primary treatment strategy for these children.

Auxin triggers pectin modification during rootlet emergence in white lupin.

Emergence of secondary roots through parental tissue is a highly controlled developmental process. Although the model plant Arabidopsis has been useful to uncover the predominant role of auxin in this process, its simple root structure is not representative of how emergence takes place in most plants, which display more complex root anatomy. White lupin is a legume crop producing structures called cluster roots, where closely spaced rootlets emerge synchronously. Rootlet primordia push their way through several cortical cell layers while maintaining the parent root integrity, reflecting more generally the lateral root emergence process in most multilayered species. In this study, we showed that lupin rootlet emergence is associated with an upregulation of cell wall pectin modifying and degrading genes under the active control of auxin. Among them, we identified LaPG3, a polygalacturonase gene typically expressed in cells surrounding the rootlet primordium and we showed that its downregulation delays emergence. Immunolabeling of pectin epitopes and their quantification uncovered a gradual pectin demethylesterification in the emergence zone, which was further enhanced by auxin treatment, revealing a direct hormonal control of cell wall properties. We also report rhamnogalacturonan-I modifications affecting cortical cells that undergo separation as a consequence of primordium outgrowth. In conclusion, we describe a model of how external tissues in front of rootlet primordia display cell wall modifications to allow for the passage of newly formed rootlets.

Rare pathogenic variants in WNK3 cause X-linked intellectual disability.

PURPOSE: WNK3 kinase (PRKWNK3) has been implicated in the development and function of the brain via its regulation of the cation-chloride cotransporters, but the role of WNK3 in human development is unknown. METHOD: We ascertained exome or genome sequences of individuals with rare familial or sporadic forms of intellectual disability (ID). RESULTS: We identified a total of 6 different maternally-inherited, hemizygous, 3 loss-of-function or 3 pathogenic missense variants (p.Pro204Arg, p.Leu300Ser, p.Glu607Val) in WNK3 in 14 male individuals from 6 unrelated families. Affected individuals had ID with variable presence of epilepsy and structural brain defects. WNK3 variants cosegregated with the disease in 3 different families with multiple affected individuals. This included 1 large family previously diagnosed with X-linked Prieto syndrome. WNK3 pathogenic missense variants localize to the catalytic domain and impede the inhibitory phosphorylation of the neuronal-specific chloride cotransporter KCC2 at threonine 1007, a site critically regulated during the development of synaptic inhibition. CONCLUSION: Pathogenic WNK3 variants cause a rare form of human X-linked ID with variable epilepsy and structural brain abnormalities and implicate impaired phospho-regulation of KCC2 as a pathogenic mechanism.

Genomic profiling of sporadic multiple meningiomas.

BACKGROUND: Multiple meningiomas (MMs) rarely occur sporadically. It is unclear whether each individual tumor in a single patient behaves similarly. Moreover, the molecular mechanisms underlying the formation of sporadic MMs and clonal formation etiology of these tumors are poorly understood. METHODS: Patients with spatially separated MMs without prior radiation exposure or a family history who underwent surgical resection of at least two meningiomas were included. Unbiased, comprehensive next generation sequencing was performed, and relevant clinical data was analyzed. RESULTS: Fifteen meningiomas and one dural specimen from six patients were included. The majority of tumors (12/15) were WHO Grade I; one patient had bilateral MMs, one of which was Grade II, while the other was Grade I. We found 11/15 of our cohort specimens were of NF2-loss subtype. Meningiomas from 5/6 patients had a monoclonal origin, with the tumor from the remaining patient showing evidence for independent clonal formation. We identified a novel case of non-NF2 mutant MM with monoclonal etiology. MMs due to a monoclonal origin did not always display a homogenous genomic profile, but rather exhibited heterogeneity due to branching evolution. CONCLUSIONS: Both NF2-loss and non-NF2 driven MMs can form due to monoclonal expansion and those tumors can acquire inter-tumoral heterogeneity through branched evolution. Grade I and II meningiomas can occur in the same patient. Thus, the molecular make-up and clinical behavior of one tumor in MMs, cannot reliably lend insight into that of the others and suggests the clinical management strategy for MMs should be tailored individually.

Impaired neurogenesis alters brain biomechanics in a neuroprogenitor-based genetic subtype of congenital hydrocephalus.

Hydrocephalus, characterized by cerebral ventricular dilatation, is routinely attributed to primary defects in cerebrospinal fluid (CSF) homeostasis. This fosters CSF shunting as the leading reason for brain surgery in children despite considerable disease heterogeneity. In this study, by integrating human brain transcriptomics with whole-exome sequencing of 483 patients with congenital hydrocephalus (CH), we found convergence of CH risk genes in embryonic neuroepithelial stem cells. Of all CH risk genes, TRIM71/lin-41 harbors the most de novo mutations and is most specifically expressed in neuroepithelial cells. Mice harboring neuroepithelial cell-specific Trim71 deletion or CH-specific Trim71 mutation exhibit prenatal hydrocephalus. CH mutations disrupt TRIM71 binding to its RNA targets, causing premature neuroepithelial cell differentiation and reduced neurogenesis. Cortical hypoplasia leads to a hypercompliant cortex and secondary ventricular enlargement without primary defects in CSF circulation. These data highlight the importance of precisely regulated neuroepithelial cell fate for normal brain-CSF biomechanics and support a clinically relevant neuroprogenitor-based paradigm of CH.

Examining Consequences Related to Unmet Care Needs Across the Long-Term Care Continuum.

OBJECTIVES: To examine how different care arrangements across the long-term care continuum are associated with experiencing unmet care need consequences (UCNCs), such as skipping meals, going without clean clothes, or taking the wrong medication. METHODS: We include older adults receiving assistance with at least one self-care, mobility, or household activity (for health/functioning reasons) in the 2015 National Health and Aging Trends Study (N = 2,388). We examine the likelihood of experiencing a UCNC across the long-term care continuum: those receiving unpaid community care only, paid community care, and residential care. Cross-sectional logistic and longitudinal multinomial logistic regression models examine if type of care arrangement in 2015 is associated with UCNCs in 2015 and change in UCNCs by 2017. RESULTS: In adjusted cross-sectional models, paid community care recipients had roughly 2 times greater odds of experiencing a UCNC in 2015 compared to those living in residential care or receiving only unpaid care. In adjusted longitudinal models, the risk of experiencing persistent UCNCs (compared to having needs met in both years) was 4.81 times higher for those receiving paid community care compared to those in residential care and 2.17 times that of those receiving unpaid care only. DISCUSSION: Older adults receiving paid care face significant and consequential gaps in care, particularly in comparison to those in other care arrangements. More attention is needed to determine how paid care arrangements can be improved and/or expanded to meet the needs of the growing number of older adults receiving paid care in the community.

The integrated multiomic diagnosis of sporadic meningiomas: a review of its clinical implications.

INTRODUCTION: Meningiomas are generally considered "benign," however, these tumors can demonstrate variability in behavior and a surprising aggressiveness with elevated rates of recurrence. The advancement of next-generation molecular technologies have led to the understanding of the genomic and epigenomic landscape of meningiomas and more recent correlations with clinical characteristics and behavior. METHODS: Based on a thorough review of recent peer-reviewed publications (PubMed) and edited texts, we provide a molecular overview of meningiomas with a focus on relevant clinical implications. RESULTS: The identification of specific somatic driver mutations has led to the classification of several major genomic subgroups, which account for more than 80% of sporadic meningiomas, and can be distinguished using noninvasive clinical variables to help guide management decisions. Other somatic genomic modifications, including non-coding alterations and copy number variations, have also been correlated with tumor characteristics. Furthermore, epigenomic modifications in meningiomas have recently been described, with DNA methylation being the most widely studied and potentially most clinically relevant. Based on these molecular insights, several clinical trials are currently underway in an effort to establish effective medical therapeutic options for meningioma. CONCLUSION: As we enhance our multiomic understanding of meningiomas, our ability to care for patients with these tumors will continue to improve. Further biological insights will lead to additional progress in precision medicine for meningiomas.

Housing Cost Burden and Health Decline Among Low- and Moderate-Income Older Renters.

OBJECTIVE: To examine the association between housing cost burden (HCB) and health decline among low- and moderate-income older renters in the United States. METHOD: Baseline data include low- and moderate-income community-dwelling older renters (N = 1,064) from the nationally representative 2015 National Health and Aging Trends Study. HCB was defined as the percentage of monthly income spent on rent, categorized as "no HCB" (<30%), "moderate HCB" (30%-49%), and "severe HCB" (≥50%). We used weighted logistic regression models to estimate whether HCB status in 2015 and change in HCB between 2015 and 2017 were associated with self-rated health decline and developing a new limitation related to activities of daily living (ADL) or instrumental activities of daily living (IADL) between 2015 and 2017. RESULTS: Older renters with severe HCB in 2015 were the most likely to develop a new ADL/IADL limitation (63.4%) over time (p < .05). The association between HCB status in 2015 and self-rated health decline was not statistically significant, but older renters with persistent HCB had 1.64 times greater odds of self-rated health decline (p < .05) and 2.01 times greater odds of developing a new ADL/IADL limitation (p < .01), compared to older renters with no HCB at baseline and follow-up. DISCUSSION: Even in the short term, HCB contributes to health decline in later life. Efforts to promote equity and healthy aging in the community must consider how to best address housing affordability among the growing population of older renters.