Air pollution nanoparticle and alpha-synuclein fibrils synergistically decrease glutamate receptor A1, depending upon nPM batch activity.

Background: Epidemiological studies have variably linked air pollution to increased risk of Parkinson's disease (PD). However, there is little experimental evidence for this association. Alpha-synuclein (α-syn) propagation plays central roles in PD and glutamate receptor A1 (GluA1) is involved in memory and olfaction function. Methods: Each mouse was exposed to one of three different batches of nano-particulate matter (nPM) (300 µg/m3, 5 h/d, 3 d/week), collected at different dates, 2017-2019, in the same urban site. After these experiments, these nPM batches were found to vary in activity. C57BL/6 female mice (3 mo) were injected with pre-formed murine α-synuclein fibrils (PFFs) (0.4 µg), which act as seeds for α-syn aggregation. Two exposure paradigms were used: in Paradigm 1, PFFs were injected into olfactory bulb (OB) prior to 4-week nPM (Batch 5b) exposure and in Paradigm 2, PFFs were injected at 4th week during 10-week nPM exposure (Batches 7 and 9). α-syn pSer129, microglia Iba1, inflammatory cytokines, and Gria1 expression were measured by immunohistochemistry or qPCR assays. Results: As expected, α-syn pSer129 was detected in ipsilateral OB, anterior olfactory nucleus, amygdala and piriform cortex. One of the three batches of nPM caused a trend for elevated α-syn pSer129 in Paradigm 1, but two other batches showed no effect in Paradigm 2. However, the combination of nPM and PFF significantly decreased Gria1 mRNA in both the ipsi- and contra-lateral OB and frontal cortex for the most active two nPM batches. Neither nPM nor PFFs alone induced responses of microglia Iba1 and expression of Gria1 in the OB and cortex. Conclusion: Exposures to ambient nPM had weak effect on α-syn propagation in the brain in current experimental paradigms; however, nPM and α-syn synergistically downregulated the expression of Gria1 in both OB and cortex.

A longitudinal study of social, religious, and spiritual capital and physical and emotional functioning in a national sample of African-Americans.

The present study builds on prior research by examining the moderating relationships between different types of capital on physical functioning, emotional functioning, and depressive symptoms using a 2.5-year longitudinal design with a national sample of African-American adults. Results indicated a significant T1 social capital × T1 religious capital interaction such that among low T1 religious capital participants, those with high T1 social capital had lower T2 physical functioning than those with lower T1 social capital. There was also a marginally significant T1 social capital × T1 spiritual capital interaction suggesting that among low T1 spiritual capital participants, those with higher T1 social capital reported a decline in depressive symptoms compared to those with lower T1 social capital. Future research and implications for intervention and policy development are discussed.

A novel automated morphological analysis of Iba1+ microglia using a deep learning assisted model.

There is growing evidence for the key role of microglial functional state in brain pathophysiology. Consequently, there is a need for efficient automated methods to measure the morphological changes distinctive of microglia functional states in research settings. Currently, many commonly used automated methods can be subject to sample representation bias, time consuming imaging, specific hardware requirements and difficulty in maintaining an accurate comparison across research environments. To overcome these issues, we use commercially available deep learning tools Aiforia® Cloud (Aifoira Inc., Cambridge, MA, United States) to quantify microglial morphology and cell counts from histopathological slides of Iba1 stained tissue sections. We provide evidence for the effective application of this method across a range of independently collected datasets in mouse models of viral infection and Parkinson's disease. Additionally, we provide a comprehensive workflow with training details and annotation strategies by feature layer that can be used as a guide to generate new models. In addition, all models described in this work are available within the Aiforia® platform for study-specific adaptation and validation.

Disability and Health in African Americans: Population Research and Implications for Occupational Therapy Community-Based Practice.

Background: Population-based research and community-based interventions are integral to occupational therapy's scope of practice, yet they are underdeveloped in actual implementation. Therefore, this paper focuses on some health challenges facing the African American population, guided by the Person-Environment-Occupation-Performance Model. Method: Using data from an observational cross-sectional nationwide telephone survey of African American adults, we examined differences between African Americans who are receiving disability payments (RDP) and those who are employed full time (FTE) on several physical health behaviors and psychosocial health indicators. We further compared the differences between African Americans RDP versus those FTE on those physical health behaviors and psychosocial health indicators across five US regions. Results: Findings suggest that African Americans RDP are engaging in fewer positive physical health behaviors and experiencing worse psychosocial health compared to their counterparts FTE. There are also nuanced regional variations in the differences between African Americans RDP and FTE in physical health behaviors and psychosocial health indicators. Conclusion: This research highlighted some health challenges of African Americans RDP and FTE using a regional lens, demonstrating the value of OT population-based research. There is a need for OT population-specific community-based practice to address the health disparities of underserved and minority populations, such as African Americans.

Heterozygous GBA D409V and ATP13a2 mutations do not exacerbate pathological α-synuclein spread in the prodromal preformed fibrils model in young mice.

Autophagic dysregulation and lysosomal impairment have been implicated in the pathogenesis of Parkinson's disease, partly due to the identification of mutations in multiple genes involved in these pathways such as GBA, SNCA, ATP13a2 (also known as PARK9), TMEM175 and LRRK2. Mutations resulting in lysosomal dysfunction are proposed to contribute to Parkinson's disease by increasing α-synuclein levels, that in turn may promote aggregation of this protein. Here, we used two different genetic models-one heterozygous for a mutated form of the GBA protein (D409V), and the other heterozygous for an ATP13a2 loss-of-function mutation, to test whether these mutations exacerbate the spread of α-synuclein pathology following injection of α-synuclein preformed fibrils in the olfactory bulb of 12-week-old mice. Contrary to our hypothesis, we found that mice harboring GBA D409V+/- and ATP13a2+/- mutations did not have exacerbated behavioral impairments or histopathology (α-synuclein, LAMP2, and Iba1) when compared to their wildtype littermates. This indicates that in the young mouse brain, neither the GBA D409V mutation or ATP13a2 loss-of-function mutation accelerate the spread of α-synuclein pathology. As a consequence, we postulate that these mutations increase Parkinson's disease risk only by acting in one of the initial, upstream events in the Parkinson's disease pathogenic process. Further, the mutations, and the molecular pathways they impact, appear to play a less important role once the pathogenic process has been triggered and therefore do not specifically influence α-synuclein pathology spread.

α-Synuclein antisense oligonucleotides as a disease-modifying therapy for Parkinson's disease.

Parkinson's disease (PD) is a prevalent neurodegenerative disease with no approved disease-modifying therapies. Multiplications, mutations, and single nucleotide polymorphisms in the SNCA gene, encoding α-synuclein (aSyn) protein, either cause or increase risk for PD. Intracellular accumulations of aSyn are pathological hallmarks of PD. Taken together, reduction of aSyn production may provide a disease-modifying therapy for PD. We show that antisense oligonucleotides (ASOs) reduce production of aSyn in rodent preformed fibril (PFF) models of PD. Reduced aSyn production leads to prevention and removal of established aSyn pathology and prevents dopaminergic cell dysfunction. In addition, we address the translational potential of the approach through characterization of human SNCA-targeting ASOs that efficiently suppress the human SNCA transcript in vivo. We demonstrate broad activity and distribution of the human SNCA ASOs throughout the nonhuman primate brain and a corresponding decrease in aSyn cerebral spinal fluid (CSF) levels. Taken together, these data suggest that, by inhibiting production of aSyn, it may be possible to reverse established pathology; thus, these data support the development of SNCA ASOs as a potential disease-modifying therapy for PD and related synucleinopathies.

An extended release GLP-1 analogue increases α-synuclein accumulation in a mouse model of prodromal Parkinson's disease.

The repurposing of drugs developed to treat type 2 diabetes for the treatment of Parkinson's disease (PD) was encouraged by the beneficial effect exerted by the glucagon-like peptide 1 (GLP-1) analogue exenatide in a phase 2 clinical trial. The effects of GLP-1 analogues have been investigated extensively using rodent toxin models of PD. However, many of the toxin-based models used lack robust α-synuclein (α-syn) pathology, akin to the Lewy bodies and neurites seen in PD. One prior study has reported a protective effect of a GLP-1 analogue on midbrain dopamine neurons following injection of α-syn preformed fibrils (PFF) into the striatum. Here, we used olfactory bulb injections of PFF as a model of prodromal PD and monitored the effect of a long-acting GLP-1 analogue on the propagation of α-syn pathology in the olfactory system. Thirteen weeks after PFF injection, mice treated with long-acting the GLP-1 analogue had a significant increase in pathological α-syn in brain regions connected to the olfactory bulb, accompanied by signs of microglia activation. Our results suggest that the nature of the neuronal insult and intrinsic properties of the targeted neuronal population markedly influence the effect of GLP-1 analogues.

T Cells Limit Accumulation of Aggregate Pathology Following Intrastriatal Injection of α-Synuclein Fibrils.

BACKGROUND: α-Synuclein (α-syn) is the predominant protein in Lewy-body inclusions, which are pathological hallmarks of α-synucleinopathies, such as Parkinson's disease (PD) and multiple system atrophy (MSA). Other hallmarks include activation of microglia, elevation of pro-inflammatory cytokines, as well as the activation of T and B cells. These immune changes point towards a dysregulation of both the innate and the adaptive immune system. T cells have been shown to recognize epitopes derived from α-syn and altered populations of T cells have been found in PD and MSA patients, providing evidence that these cells can be key to the pathogenesis of the disease.ObjectiveTo study the role of the adaptive immune system with respect to α-syn pathology. METHODS: We injected human α-syn preformed fibrils (PFFs) into the striatum of immunocompromised mice (NSG) and assessed accumulation of phosphorylated α-syn pathology, proteinase K-resistant α-syn pathology and microgliosis in the striatum, substantia nigra and frontal cortex. We also assessed the impact of adoptive transfer of naïve T and B cells into PFF-injected immunocompromised mice. RESULTS: Compared to wildtype mice, NSG mice had an 8-fold increase in phosphorylated α-syn pathology in the substantia nigra. Reconstituting the T cell population decreased the accumulation of phosphorylated α-syn pathology and resulted in persistent microgliosis in the striatum when compared to non-transplanted mice. CONCLUSION: Our work provides evidence that T cells play a role in the pathogenesis of experimental α-synucleinopathy.

Meaning in Life Predicts Decreased Depressive Symptoms and Increased Positive Affect over Time but Does Not Buffer Stress Effects in a National Sample of African-Americans.

Few studies have specifically focused on meaning in life in African Americans and many important questions remain, including whether effects of meaning in life are direct or moderated by levels of stress. In a national sample of 909 African Americans, we tested meaning in life as a prospective predictor of changes in depressive symptoms and positive affect over a 2.5-year period. Controlling for demographics and hassles, meaning in life predicted decreased depressive symptoms and increased positive affect across the span of 2.5 years. Moderation effects were not found for hassles, age, or income. Gender moderated the effect of meaning on positive affect such that effects were stronger for women than for men. These results suggest that, for African Americans, meaning in life appears to robustly protect against future depressive symptoms and promote positive affect over time unaffected by amount of stress experienced or most demographic factors.

Do neighborhood characteristics contribute beyond individual demographics to cancer control behaviors among African American adults?

BACKGROUND: Recent years have seen increased interest in the role of neighborhood factors in chronic diseases such as cancers. Less is known about the role of neighborhood factors beyond individual demographics such as age or education. It is particularly important to examine neighborhood effects on health among African American men and women, considering the disproportionate impact of cancer on this group. This study evaluated the unique contribution of neighborhood characteristics (e.g., racial/ethnic diversity, income) beyond individual demographics, to cancer control behaviors in African American men and women. METHODS: Individual-level data were drawn from a national survey (N = 2,222). Participants' home addresses were geocoded and merged with neighborhood data from the American Community Survey. Multi-level regressions examined the unique contribution of neighborhood characteristics beyond individual demographics, to a variety of cancer risk, prevention, and screening behaviors. RESULTS: Neighborhood racial/ethnic diversity, median income, and percentage of home ownership made modest significant contributions beyond individual factors, in particular to smoking status where these factors were associated with lower likelihood of smoking (ps < .05). Men living in neighborhoods with older residents, and greater income and home ownership were significantly more likely to report prostate specific antigen testing (ps < .05). Regional analyses suggested different neighborhood factors were associated with smoking status depending on the region. CONCLUSION: Findings provide a more nuanced understanding of the interplay of social determinants of health and neighborhood social environment among African American men and women, with implications for cancer control interventions to eliminate cancer disparities.

Inhibiting the mitochondrial pyruvate carrier does not ameliorate synucleinopathy in the absence of inflammation or metabolic deficits.

Epidemiological studies suggest a link between type-2 diabetes and Parkinson's disease (PD) risk. Treatment of type-2 diabetes with insulin sensitizing drugs lowers the risk of PD. We previously showed that the insulin sensitizing drug, MSDC-0160, ameliorates pathogenesis in some animal models of PD. MSDC-0160 reversibly binds the mitochondrial pyruvate carrier (MPC) protein complex, which has an anti-inflammatory effect and restores metabolic deficits. Since PD is characterized by the deposition of α-synuclein (αSyn), we hypothesized that inhibiting the MPC might directly inhibit αSyn aggregation in vivo in mammals. To answer if modulation of MPC can reduce the development of αSyn assemblies, and reduce neurodegeneration, we treated two chronic and progressive mouse models; a viral vector-based αSyn overexpressing model and a pre-formed fibril (PFF) αSyn seeding model with MSDC-0160. These two models present distinct types of αSyn pathology but lack inflammatory or autophagy deficits. Contrary to our hypothesis, we found that a modulation of MPC in these models did not reduce the accumulation of αSyn aggregates or mitigate neurotoxicity. Instead, MSDC-0160 changed the post-translational modification and aggregation features of αSyn. These results are consistent with the lack of a direct effect of MPC modulation on synuclein clearance in these models.

A longitudinal examination of social support as a mediator of the personality-health relationship in a national sample of African Americans.

The present study investigates whether social support mediates the relationship between personality traits and health among African Americans over a five-year period, filling a gap in the literature on longitudinal tests of the personality-health association. Data were collected from a national probability sample of African American adults (N = 200). Personality was assessed at Time 1 (T1), social support was assessed 2.5 years later (T2), and physical functioning was examined 5 years (T3) after T1. Telephone surveys included measures of the Five Factor Model personality traits (T1), social support (T2), and physical functioning (T3). Results suggested that relationships between the T1 personality traits and T3 physical functioning were not mediated by T2 social support. Secondary analyses found that among all T1 personality traits, higher openness and lower neuroticism uniquely predicted higher T2 social support. Further, among T1 personality traits, higher conscientiousness uniquely predicted better T3 physical functioning. This information may be useful to healthcare providers and community members in developing prevention and intervention strategies for African Americans.

Microglia affect α-synuclein cell-to-cell transfer in a mouse model of Parkinson's disease.

BACKGROUND: Cell-to-cell propagation of α-synuclein (α-syn) aggregates is thought to contribute to the pathogenesis of Parkinson's disease (PD) and underlie the spread of α-syn neuropathology. Increased pro-inflammatory cytokine levels and activated microglia are present in PD and activated microglia can promote α-syn aggregation. However, it is unclear how microglia influence α-syn cell-to-cell transfer. METHODS: We developed a clinically relevant mouse model to monitor α-syn prion-like propagation between cells; we transplanted wild-type mouse embryonic midbrain neurons into a mouse striatum overexpressing human α-syn (huα-syn) following adeno-associated viral injection into the substantia nigra. In this system, we depleted or activated microglial cells and determined the effects on the transfer of huα-syn from host nigrostriatal neurons into the implanted dopaminergic neurons, using the presence of huα-syn within the grafted cells as a readout. RESULTS: First, we compared α-syn cell-to-cell transfer between host mice with a normal number of microglia to mice in which we had pharmacologically ablated 80% of the microglia from the grafted striatum. With fewer host microglia, we observed increased accumulation of huα-syn in grafted dopaminergic neurons. Second, we assessed the transfer of α-syn into grafted neurons in the context of microglia activated by one of two stimuli, lipopolysaccharide (LPS) or interleukin-4 (IL-4). LPS exposure led to a strong activation of microglial cells (as determined by microglia morphology, cytokine production and an upregulation in genes involved in the inflammatory response in the LPS-injected mice by RNA sequencing analysis). LPS-injected mice had significantly higher amounts of huα-syn in grafted neurons. In contrast, injection of IL-4 did not change the proportion of grafted dopamine neurons that contained huα-syn relative to controls. As expected, RNA sequencing analysis on striatal tissue revealed differential gene expression between LPS and IL-4-injected mice; with the genes upregulated in tissue from mice injected with LPS including several of those involved in an inflammatory response. CONCLUSIONS: The absence or the hyperstimulation of microglia affected α-syn transfer in the brain. Our results suggest that under resting, non-inflammatory conditions, microglia modulate the transfer of α-syn. Pharmacological regulation of neuroinflammation could represent a future avenue for limiting the spread of PD neuropathology.

Unique contribution of education to behavioral and psychosocial antecedents of health in a national sample of African Americans.

Education has demonstrated consistent links with many aspects of physical health and is theorized to relate to a variety of behavioral and psychosocial antecedents of health that may ultimately account for these associations. However, many of these associations and the extent to which they manifest specifically for African Americans have not been thoroughly tested. We examined associations of education-distinct from income-with established behavioral and psychosocial antecedents of health in a national sample of African Americans. Education favorably related to many behavioral (e.g., fruit/vegetable intake, lifetime smoking) and psychosocial (e.g., self-efficacy, personality traits, self-esteem, psychological well-being) antecedents of health, but not to all. Some evidence of stronger salutary relations of education for women was found. Results suggest that, for African Americans, education is generally favorably associated with an array of behavioral and psychosocial antecedents of physical health, partially explaining health disparities and providing a point of intervention moving forward.

α-Synuclein conformational strains spread, seed and target neuronal cells differentially after injection into the olfactory bulb.

Alpha-synuclein inclusions, the hallmarks of synucleinopathies, are suggested to spread along neuronal connections in a stereotypical pattern in the brains of patients. Ample evidence now supports that pathological forms of alpha-synuclein propagate in cell culture models and in vivo in a prion-like manner. However, it is still not known why the same pathological protein targets different cell populations, propagates with different kinetics and leads to a variety of diseases (synucleinopathies) with distinct clinical features. The aggregation of the protein alpha-synuclein yields different conformational polymorphs called strains. These strains exhibit distinct biochemical, physical and structural features they are able to imprint to newly recruited alpha-synuclein. This had led to the view that the clinical heterogeneity observed in synucleinopathies might be due to distinct pathological alpha-synuclein strains.To investigate the pathological effects of alpha-synuclein strains in vivo, we injected five different pure strains we generated de novo (fibrils, ribbons, fibrils-65, fibrils-91, fibrils-110) into the olfactory bulb of wild-type female mice. We demonstrate that they seed and propagate pathology throughout the olfactory network within the brain to different extents. We show strain-dependent inclusions formation in neurites or cell bodies. We detect thioflavin S-positive inclusions indicating the presence of mature amyloid aggregates.In conclusion, alpha-synuclein strains seed the aggregation of their cellular counterparts to different extents and spread differentially within the central nervous system yielding distinct propagation patterns. We provide here the proof-of-concept that the conformation adopted by alpha-synuclein assemblies determines their ability to amplify and propagate in the brain in vivo. Our observations support the view that alpha-synuclein polymorphs may underlie different propagation patterns within human brains.

Identifying and Understanding Communities Using Twitter to Connect About Depression: Cross-Sectional Study.

BACKGROUND: Depression is the leading cause of diseases globally and is often characterized by a lack of social connection. With the rise of social media, it is seen that Twitter users are seeking Web-based connections for depression. OBJECTIVE: This study aimed to identify communities where Twitter users tweeted using the hashtag #MyDepressionLooksLike to connect about depression. Once identified, we wanted to understand which community characteristics correlated to Twitter users turning to a Web-based community to connect about depression. METHODS: Tweets were collected using NCapture software from May 25 to June 1, 2016 during the Mental Health Month (n=104) in the northeastern United States and Washington DC. After mapping tweets, we used a Poisson multilevel regression model to predict tweets per community (county) offset by the population and adjusted for percent female, percent population aged 15-44 years, percent white, percent below poverty, and percent single-person households. We then compared predicted versus observed counts and calculated tweeting index values (TIVs) to represent undertweeting and overtweeting. Last, we examined trends in community characteristics by TIV using Pearson correlation. RESULTS: We found significant associations between tweet counts and area-level proportions of females, single-person households, and population aged 15-44 years. TIVs were lower than expected (TIV 1) in eastern, seaboard areas of the study region. There were communities tweeting as expected in the western, inland areas (TIV 2). Counties tweeting more than expected were generally scattered throughout the study region with a small cluster at the base of Maine. When examining community characteristics and overtweeting and undertweeting by county, we observed a clear upward gradient in several types of nonprofits and TIV values. However, we also observed U-shaped relationships for many community factors, suggesting that the same characteristics were correlated with both overtweeting and undertweeting. CONCLUSIONS: Our findings suggest that Web-based communities, rather than replacing physical connection, may complement or serve as proxies for offline social communities, as seen through the consistent correlations between higher levels of tweeting and abundant nonprofits. Future research could expand the spatiotemporal scope to confirm these findings.

Metabolomic Profiling of Bile Acids in an Experimental Model of Prodromal Parkinson's Disease.

For people with Parkinson's disease (PD), considered the most common neurodegenerative disease behind Alzheimer's disease, accurate diagnosis is dependent on many factors; however, misdiagnosis is extremely common in the prodromal phases of the disease, when treatment is thought to be most effective. Currently, there are no robust biomarkers that aid in the early diagnosis of PD. Following previously reported work by our group, we accurately measured the concentrations of 18 bile acids in the serum of a prodromal mouse model of PD. We identified three bile acids at significantly different concentrations (p < 0.05) when mice representing a prodromal PD model were compared with controls. These include ω-murichoclic acid (MCAo), tauroursodeoxycholic acid (TUDCA) and ursodeoxycholic acid (UDCA). All were down-regulated in prodromal PD mice with TUDCA and UDCA at significantly lower levels (17-fold and 14-fold decrease, respectively). Using the concentration of three bile acids combined with logistic regression, we can discriminate between prodromal PD mice from control mice with high accuracy (AUC (95% CI) = 0.906 (0.777⁻1.000)) following cross validation. Our study highlights the need to investigate bile acids as potential biomarkers that predict PD and possibly reflect the progression of manifest PD.

Personality, Social Capital, and Depressive Symptomatology Among African Americans.

The present study examined the relationship between social capital and depressive symptoms and the moderating role of the Big Five personality constructs in a national sample of African American adults. Data were collected from a national probability sample of 803 African American men and women using a telephone survey including measures of the Big Five personality traits, social capital, and depressive symptomatology. Most interestingly, there was evidence for Personality X Social Capital interactions on depressive symptoms. Higher social capital was related to lower depressive symptomology among persons with low conscientiousness, low extraversion, or high neuroticism. However, social capital was significantly but not as strongly related to depressive symptoms among those with high conscientiousness, high extraversion, or low neuroticism. This study reinforces the importance of personality traits when considering potential protective health effects of social capital in understanding depressive symptoms. This information may be useful to practitioners and community members in prevention and treatment.

Biochemical Profiling of the Brain and Blood Metabolome in a Mouse Model of Prodromal Parkinson's Disease Reveals Distinct Metabolic Profiles.

Parkinson's disease is the second most common neurodegenerative disease. In the vast majority of cases the origin is not genetic and the cause is not well understood, although progressive accumulation of α-synuclein aggregates appears central to the pathogenesis. Currently, treatments that slow disease progression are lacking, and there are no robust biomarkers that can facilitate the development of such treatments or act as aids in early diagnosis. Therefore, we have defined metabolomic changes in the brain and serum in an animal model of prodromal Parkinson's disease. We biochemically profiled the brain tissue and serum in a mouse model with progressive synucleinopathy propagation in the brain triggered by unilateral injection of preformed α-synuclein fibrils in the olfactory bulb. In total, we accurately identified and quantified 71 metabolites in the brain and 182 in serum using 1H NMR and targeted mass spectrometry, respectively. Using multivariate analysis, we accurately identified which metabolites explain the most variation between cases and controls. Using pathway enrichment analysis, we highlight significantly perturbed biochemical pathways in the brain and correlate these with the progression of the disease. Furthermore, we identified the top six discriminatory metabolites and were able to develop a model capable of identifying animals with the pathology from healthy controls with high accuracy (AUC (95% CI) = 0.861 (0.755-0.968)). Our study highlights the utility of metabolomics in identifying elements of Parkinson's disease pathogenesis and for the development of early diagnostic biomarkers of the disease.

Fruit and Vegetable Consumption, and Physical Activity with Partner and Parental Status in African American Adults.

OBJECTIVES: The purpose of this study was to examine the relationships between partner and parental status and self-reported weekly fruit and vegetable consumption and level of physical activity in African American adults. METHODS: A national sample of 2,370 African Americans participated in a telephone survey. Demographic data were collected and compared with fruit and vegetable consumption and physical activity responses. RESULTS: When controlling for age (mean age = 53.6 ± 14.8 years) and education level, having children in the household was associated with greater fruit consumption. Being partnered was associated with moderate physical activity weekly for a higher percentage of women, and yet a shorter duration of minutes of moderate physical activity weekly for both women and men. Males (38.2% of the sample) reported being more physically active and females (61.8% of the sample) reported eating more fruits and vegetables. CONCLUSIONS: By understanding the role of partner and parental status in relation to healthy lifestyle for African Americans, family scientists and health care practitioners may be able to target the needs of this population to help prevent obesity and chronic illness.