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University of Southern California · Doctor of Physical Therapy Program
Active 2022–2026
Aimee M. Diaz, PT, DPT, SCS, ATC, is an Associate Professor of Clinical Physical Therapy at the USC Division of Biokinesiology and Physical Therapy. She serves as the Director of the Sports Physical Therapy Fellowship in Division I Athletics and is the Clinic Director at USC Physical Therapy on the University Park Campus. Dr. Diaz provides patient care to faculty, staff, students, and community patients, overseeing physical therapy outreach services on campus. She is a board-certified sports physical therapist with extensive experience treating patients with sports-related injuries, orthopedic disorders, post-surgical rehabilitation, and facilitating functional return to sport. Her clinical expertise includes work with Division I Athletics, extreme sports, and the female athlete, and she also treats women’s health-related disorders. Dr. Diaz is a member of the American Academy of Sports Physical Therapy and the Academy of Pelvic Health Physical Therapy, and she is certified as an athletic trainer through the Board of Certification. She has been involved in clinical and academic pursuits, including serving as the director of the USC Sports Division I Physical Therapy Fellowship, collaborating with USC and UCLA Athletic Departments, and providing event sports medicine coverage. Additionally, she was the director of the USC Sports Physical Therapy Residency Program from 2009 until 2024 and has been an invited speaker and presenter at various conferences.
Open Science Framework · 2026-01-01
Constantinos Sioutas
University of Southern California
William J. Mack
University of Southern California
Caleb E. Finch
Kristina Shkirkova
Hongqiao Zhang
PhdFit ranks faculty by your research interests, methods, and publications — grounded in their actual work, not templates.
Stroke · 2024-02-01
Background: Exposure to ambient air pollution causes neuroinflammation and white matter (WM) damage. In patients with preexisting cerebrovascular disease, pollution exposure can compound underlying pathology and may accelerate functional decline. Major mechanisms of this toxicity are microglial reactivity and oxidative stress. We therefore hypothesized that attenuation of the Toll-like receptor 4 (TLR4)-dependent microglial response would significantly decrease oxidative WM damage in a joint experimental model of pollutant exposure and chronic cerebral hypoperfusion modeled by surgical bilateral carotid artery stenosis (BCAS). Methods: Inducible microglial/macrophage-specific TLR4 deletion was achieved using a Tamoxifen-induced Cx3cr1CreER+/- mouse model. Male and female Cx3cr1CreER+/- mice treated with tamoxifen (i-mTLR4-ko) or corn oil (control) were exposed to 120 hours of filtered air (FA) or aerosolized diesel exhaust particulate (DEP), and 30 days of BCAS or sham surgery using a factorial design. The 8 experimental groups were: 1) control/FA (n=10), 2) control/DEP (n=10), 3) control/FA + BCAS (n=9), 4) control/DEP+BCAS (n=10), 5) i-mTLR4-ko/FA (n=9), 6) i-mTLR4-ko/DEP (n=8), 7) i-mTLR4-ko/FA + BCAS (n=8), and 8) i-mTLR4-ko/DEP+BCAS (n=10). Immunofluorescence was used to identify 4-HNE and 8-OHdG expression in the corpus callosum (CC). Results: While control mice showed elevations of 4-HNE in the CC after DEP (p<0.01) and DEP+BCAS (p<0.0001), i-mTLR4-ko prevented this change (Figure 1). While control mice exhibited a rise in 8-OHdG in the CC after DEP+BCAS (p<0.05), i-mTLR4-ko prevented this rise. Conclusions: We demonstrate that i-mTLR4-ko is sufficient to abate major elevations in oxidative stress markers in WM after DEP and BCAS exposures. This suggests a potential role for therapies targeting TLR4 signaling to minimize pollution-associated neurotoxicity, particularly in the setting of cerebral hypoperfusion.
Stroke · 2024 · 15 citations
BACKGROUND: Air pollution particulate matter exposure and chronic cerebral hypoperfusion (CCH) contribute to white matter toxicity through shared mechanisms of neuroinflammation, oxidative stress, and myelin breakdown. Prior studies showed that exposure of mice to joint particulate matter and CCH caused supra-additive injury to corpus callosum white matter. This study examines the role of TLR4 (toll-like receptor 4) signaling in mediating neurotoxicity and myelin damage observed in joint particulate matter and CCH exposures. METHODS: Experiments utilized a novel murine model of inducible monocyte/microglia-specific TLR4 knockout (i-mTLR4-ko). Bilateral carotid artery stenosis (BCAS) was induced surgically to model CCH. TLR4-intact (control) and i-mTLR4-ko mice were exposed to 8 weeks of either aerosolized diesel exhaust particulate (DEP) or filtered air (FA) in 8 experimental groups: (1) control/FA (n=10), (2) control/DEP (n=10), (3) control/FA+BCAS (n=9), (4) control/DEP+BCAS (n=10), (5) i-mTLR4-ko/FA (n=9), (6) i-mTLR4-ko/DEP (n=8), (7) i-mTLR4-ko/FA+BCAS (n=8), and (8) i-mTLR4-ko/DEP+BCAS (n=10). Corpus callosum levels of 4-hydroxynonenal, 8-Oxo-2'-deoxyguanosine, Iba-1 (ionized calcium-binding adapter molecule 1), and dMBP (degraded myelin basic protein) were assayed via immunofluorescence to measure oxidative stress, neuroinflammation, and myelin breakdown, respectively. RESULTS: <0.05). I-mTLR4 knockout attenuated responses to DEP/BCAS for all markers. CONCLUSIONS: i-mTLR4-ko markedly reduced neuroinflammation and oxidative stress and attenuated white matter degradation following DEP and CCH exposures. This suggests a potential role for targeting TLR4 signaling in individuals with vascular cognitive impairment, particularly those exposed to substantial ambient air pollution.
Neurosurgery · 2024-03-15
INTRODUCTION: Air pollution is recognized as a neurotoxin which damages white matter and increases the risk of cognitive decline. Our previous work in a murine model found that air pollution in the setting of chronic cerebral hypoperfusion (CCH) leads to a synergistic deleterious effect on white matter. Air pollution studies have shown that increased microglial activation was associated with neurotoxicity. We hypothesize that inhibition of a microglial-specific TLR4 pathway will decrease the neurodegenerative effects that normally result from combined CCH and air pollution. METHODS: Our air pollution model used eight weeks of standardized Diesel Exhaust Particles (DEP) from National Institute of Science and Technology (DEP NIST2975). We performed bilateral carotid stenosis (BCAS) surgery to induce CCH using Wild Type (WT) and TLR4 flx/flx (CX3CR1CreER +/-) (TLR4-KD) in 2-month-old male mice. WT and TLR4-KD mice were randomized into eight groups as follows: WT-filtered air (FA), WT-DEP, WT-FA-BCAS, WT-DEP-BCAS, TLR4-KD-FA, TLR4-KD-DEP, TLR4-KD-FA-BCAS, and TLR4-KD-DEP-BCAS. Neurotoxicity was quantified with immunohistochemistry of degraded myelin basic protein (dMBP), ionized calcium-binding adaptor molecule-1 (Iba-1), and complement (C5a). RESULTS: DEP exposure resulted in increased white matter injury in corpus callosum (dMBP), worsened by the presence of CCH (p = 0.004) and significantly attenuated by TLR4-KD (p = 0.005). DEP exposure resulted in increased white matter microglial activation (Iba-1), worsened by the presence of CCH (p < 0.0001) and significantly attenuated by TLR4-KD (p = 0.04).DEP exposure resulted in increased white matter complement activation (C5a), worsened by the presence of CCH (p < 0.0001) and significantly attenuated by TLR4-KD (p < 0.0001). CONCLUSIONS: Microglial-specific TLR4-KD reduces air pollution-induced neurotoxicity measured by white matter injury, microglial activation, and neuroinflammation.
Magnetic resonance imaging of white matter response to diesel exhaust particles
Research Square (Research Square) · 2023 · 3 citations
for 200 hours. Ex-vivo MRI analysis and fractional anisotropy (FA)-aided white matter tractography were conducted to study the effect of DEP exposure on the brain white matter tracts. Immunohistochemistry was used to assess myelin and axonal structure. DEP exposure for 8 weeks altered myelin composition in multiple regions. Diffusion tensor imaging (DTI) showed decreased FA in the corpus callosum (30%), external capsule (15%), internal capsule (15%), and cingulum (31 %). Separate immunohistochemistry analyses confirmed prior findings. Myelin basic protein (MBP) was decreased (corpus callosum: 28%, external capsule: 29%), and degraded MPB increased (corpus callosum: 32%, external capsule: 53%) in the DEP group. White matter is highly susceptible to chronic DEP exposure. This study demonstrates the utility of DTI as a neuroanatomical tool in the context of air pollution and white matter myelin vulnerability.
Alzheimer s & Dementia · 2023-12-01
Abstract Background Epidemiological studies show chronic exposure to air pollution accelerates cognitive decline and increase AD risk. In mouse models, brain accumulation of amyloid beta (Aβ) is enhanced by air pollution. Pharmacological approaches show benefit of γ‐secretase modulation (GSM; BPN‐15606), decreasing Aβ42 and amyloid plaques in mouse brain. We hypothesize that GSM will limit Aβ42 production during air pollution exposure in the diesel exhaust particle (DEP) model. Method C57BL/6 mice were exposed to DEP for 8 weeks. DEP from National Institute of Science and Technology (NIST 2975) was suspended in water and re‐aerosolized for 5 hr/day at concentration of 100 µg/m 3 . GSM was mixed into chow (10mg/day dose). Experimental groups were filtered air (FA), DEP, FA+GSM, and DEP+GSM; proteins from soluble fraction of cerebral cortex were analyzed by immunoblots. Result GSM alone increased amyloid precursor protein (APP) and the Aβ38 peptide. Air pollution (DEP) increased APP, with no further change in DEP+GSM. PSEN1, key enzyme for γ‐secretase function, decreased with DEP+GSM, along with the Aβ42 peptide and the Aβ42/40 ratio. Conclusion During exposure to DEP, GSM decreased Aβ42 and the ratio of Aβ42/40. These results suggest that γ‐secretase modulation is beneficial during air pollution, preventing Aβ42 increases.
Alzheimer s & Dementia · 2022-12-01
Abstract Background Exposure to urban air pollution particles is strongly associated with higher risks of accelerated cognitive decline, cerebral atrophy, and dementia in multiple population studies. Among possible mechanisms is the decrease of neurotrophins, shown for BDNF in human exposures, which have critical roles in regulating adult neurogenesis and synaptic plasticity. Method C57BL/6 mice were exposed to nano‐sized particulate matter (nPM, batch nPM2016a) from urban traffic air pollution for 8 weeks and the mRNAs of neurotrophins and receptors in mouse brain were measured by qPCR assay and neural stem cells measured by immunohistochemistry. Result nPM exposure altered mRNA levels of neurotrophin genes ( Ngf , Bdnf , Ntf‐3 and Ntf‐4/5 ) with brain region‐specificity. In cerebral cortex (CX), Ngf and Ntf‐3 were decreased (17% and 29% respectively), Ntf‐4/5 increased (78%), and Bdnf unchanged. In hippocampus (HP), Bdnf and Ntf‐4/5 were decreased (40% and 38% respectively) while Ngf and NTF‐3 unchanged. In olfactory bulb (OB), only Bdnf was decreased (10%). The mRNAs of neurotrophin receptors ( Trka , Trkb , Trkc and p75Ntr ) in CX, HP and OB were less responsive to nPM exposure, and only shown by OB with 22% decrease of p75Ntr and 14% decrease of Vgr (VGF nerve growth factor inducible). Exposure to nPM increased the quiescence of neural stem cells in hippocampal SGZ by IHC assay (Control 69.3% VS nPM 76.6%, P = 0.02), but did not alter the total number of neural stem cells. . Conclusion Chronic air pollution exposure altered neurotrophin signaling with factor‐ and brain region‐specificity, and increased neural stem cell quiescence.
Neurotoxicity of Diesel Exhaust Particles
Journal of Alzheimer s Disease · 2022 · 17 citations
BACKGROUND: Air pollution particulate matter (PM) is strongly associated with risks of accelerated cognitive decline, dementia and Alzheimer's disease. Ambient PM batches have variable neurotoxicity by collection site and season, which limits replicability of findings within and between research groups for analysis of mechanisms and interventions. Diesel exhaust particles (DEP) offer a replicable model that we define in further detail. OBJECTIVE: Define dose- and time course neurotoxic responses of mice to DEP from the National Institute of Science and Technology (NIST) for neurotoxic responses shared by DEP and ambient PM. METHODS: For dose-response, adult C57BL/6 male mice were exposed to 0, 25, 50, and 100μg/m3 of re-aerosolized DEP (NIST SRM 2975) for 5 h. Then, mice were exposed to 100μg/m3 DEP for 5, 100, and 200 h and assayed for amyloid-β peptides, inflammation, oxidative damage, and microglial activity and morphology. RESULTS: DEP exposure at 100μg/m3 for 5 h, but not lower doses, caused oxidative damage, complement and microglia activation in cerebral cortex and corpus callosum. Longer DEP exposure for 8 weeks/200 h caused further oxidative damage, increased soluble Aβ, white matter injury, and microglial soma enlargement that differed by cortical layer. CONCLUSION: Exposure to 100μg/m3 DEP NIST SRM 2975 caused robust neurotoxic responses that are shared with prior studies using DEP or ambient PM0.2. DEP provides a replicable model to study neurotoxic mechanisms of ambient PM and interventions relevant to cognitive decline and dementia.
SHORT-TERM DIESEL EXHAUST PARTICLE NEUROTOXICITY MEDIATED BY TLR4 ACROSS AGE AND SEX
Innovation in Aging · 2022-11-01
Abstract Experimental animal exposures show neurotoxic effects of diesel in young mice even after short-term exposures. We hypothesize that neuroinflammatory effects of diesel exhaust particles (DEP) are mediated by toll-like receptor 4 (TLR4) activation in brain microglia. We studied both sexes of young (2 months) and middle-aged (18 months) TLR4 flx/flx (CX3CR1CreER +/-) mice, in which macrophage-specific TLR4 deletion is induced by tamoxifen. DEP from National Institute of Science and Technology (NIST 2975) was suspended in pure water and re-aerosolized for 5 hr exposure at 100 µg/m3 concentration. Experimental groups were Filtered Air+Corn Oil, DEP+Corn Oil, Filtered Air+Tamoxifen, DEP+Tamoxifen. We studied markers of inflammation, oxidative stress, and microglia activation in the white matter of corpus callosum. At baseline, middle-aged mice showed higher levels of microglia activation (Iba-1), complement activation (C5, C5a), and oxidative stress (8-OHdG, 4HNE). DEP significantly increased microglial activation, inflammation, and oxidative stress. TLR4 knockdown showed a rescue effect in DEP group for Iba-1 and 8-OHdG in young but not in middle-aged mice. Both C5a and 4HNE were rescued by TLR4 knockdown in young and middle-aged mice, possibly with less robust effects in older mice. No significant sex effects were observed. Middle-aged mice have higher levels of baseline white matter inflammation and oxidative stress. DEP exposure caused robust neuroinflammatory and oxidative responses in white matter across ages. TLR4 knockdown attenuated DEP caused neuroinflammatory and oxidative responses, suggesting that microglia play an important role in DEP neurotoxicity.
Wendy J. Mack
Southern California University for Professional Studies
Max Thorwald
University of Southern California
Nathan Zhang
University of Southern California