Advances in Alzheimer’s Disease最新文献

Handbook of Microbiome and Gut-Brain-Axis in Alzheimer’s Disease 阿尔茨海默病微生物组和肠-脑轴手册

Advances in Alzheimer’s Disease Pub Date : 2022-07-01 DOI: 10.3233/aiad9

引用次数: 1

Alzheimer’s Disease and Air Pollution 阿尔茨海默病和空气污染

Advances in Alzheimer’s Disease Pub Date : 2021-04-16 DOI: 10.3233/aiad8

引用次数: 0

Air Pollution as Risk Factor for Mental Disorders: In Search for a Possible Link with Alzheimer’s Disease and Schizophrenia 空气污染是精神障碍的危险因素:寻找与阿尔茨海默病和精神分裂症的可能联系

Advances in Alzheimer’s Disease Pub Date : 1900-01-01 DOI: 10.3233/aiad210043

L. Attademo, F. Bernardini

{"title":"Air Pollution as Risk Factor for Mental Disorders: In Search for a Possible Link with Alzheimer’s Disease and Schizophrenia","authors":"L. Attademo, F. Bernardini","doi":"10.3233/aiad210043","DOIUrl":"https://doi.org/10.3233/aiad210043","url":null,"abstract":"As a global problem that has increasingly been causing worldwide concern, air pollution poses a significant and serious environmental risk to health. Risks of cardiovascular and respiratory diseases, as well as various types of cancer, have been consistently associated with the exposure to air pollutants. More recently, various studies have also shown that the central nervous system is also attacked by air pollution. Air pollution appears to be strongly associated with a higher risk of cognitive defects, neurodevelopmental (e.g., schizophrenia) and neurodegenerative (e.g., Alzheimer’s disease) disorders. Subjects with schizophrenia, as well as subjects with Alzheimer’s disease, experience a variety of neuropsychological deficits and cognitive impairments. This determines an adverse effect on social and professional functioning, and it contributes to the long-term disease burden. However, no final conclusions have been drawn on the matter of the direct relationship between schizophrenia and Alzheimer’s disease. In recent years, the topic of urbanicity and mental health has become increasingly important. Urban exposure to environmental toxins and pollution is currently described as a reliable risk factor for schizophrenia and other psychoses, and it has been demonstrated more and more how exposure to air pollutants is associated with increased risk of dementia. Pathways by which air pollution can target and damage the brain, leading to an increased risk for developing schizophrenia and Alzheimer’s disease, are multiple and complex. Results from epidemiological studies suggest potential associations, but are still insufficient to confirm causality. Further studies are needed in order to verify this hypothesis. And if confirmed, the clinical implications could be of substantial relevance for both public and mental health.","PeriodicalId":294723,"journal":{"name":"Advances in Alzheimer’s Disease","volume":"154 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116779001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cerebrospinal Fluid Biomarkers in Highly Exposed PM2.5 Urbanites: The Risk of Alzheimer’s and Parkinson’s Diseases in Young Mexico City Residents 高暴露PM2.5城市居民的脑脊液生物标志物:年轻墨西哥城居民患阿尔茨海默病和帕金森病的风险

Advances in Alzheimer’s Disease Pub Date : 1900-01-01 DOI: 10.3233/aiad210039

L. Calderón-Garcidueñas, J. Ávila-Ramírez, A. Calderón-Garcidueñas, T. González-Heredia, Hilda Acuña-Ayala, Chih-Kai Chao, Charles Thompson, R. Ruiz-Ramos, Victor Cortés-González, Luz Martínez-Martínez, Mario Alberto García-Pérez, J. Reis, P. Mukherjee, R. Torres-Jardón, I. Lachmann

{"title":"Cerebrospinal Fluid Biomarkers in Highly Exposed PM2.5 Urbanites: The Risk of Alzheimer’s and Parkinson’s Diseases in Young Mexico City Residents","authors":"L. Calderón-Garcidueñas, J. Ávila-Ramírez, A. Calderón-Garcidueñas, T. González-Heredia, Hilda Acuña-Ayala, Chih-Kai Chao, Charles Thompson, R. Ruiz-Ramos, Victor Cortés-González, Luz Martínez-Martínez, Mario Alberto García-Pérez, J. Reis, P. Mukherjee, R. Torres-Jardón, I. Lachmann","doi":"10.3233/aiad210039","DOIUrl":"https://doi.org/10.3233/aiad210039","url":null,"abstract":"Exposure to fine particulate matter (PM2.5) and ozone (O3) above US EPA standards is associated with Alzheimer’s disease (AD) risk, while Mn toxicity induces parkinsonism. Mexico City Metropolitan Area (MCMA) children have pre- and postnatal sustained and high exposures to PM2.5, O3, polycyclic aromatic hydrocarbons, and metals. Young MCMA residents exhibit frontal tau hyperphosphorylation and amyloid-β (Aβ)1–42 diffuse plaques, and aggregated and hyperphosphorylated α-synuclein in olfactory nerves and key brainstem nuclei. We measured total prion protein (TPrP), total tau (T-tau), tau phosphorylated at threonine 181 (P-Tau), Aβ1–42, α-synuclein (t-α-syn and d-α-synuclein), BDNF, insulin, leptin, and/or inflammatory mediators, in 129 normal CSF samples from MCMA and clean air controls. Aβ1–42 and BDNF concentrations were significantly lower in MCMA children versus controls (p = 0.005 and 0.02, respectively). TPrP increased with cumulative PM2.5 up to 5 μg/m3 and then decreased, regardless of cumulative value or age (R2 = 0.56). TPrP strongly correlated with T-Tau and P-Tau, while d-α-synuclein showed a significant correlation with TNFα, IL10, and IL6 in MCMA children. Total synuclein showed an increment in childhood years related to cumulated PM2.5, followed by a decrease after age 12 years R2 = 0.47), while d-α-synuclein exhibited a tendency to increase with cumulated PM2.5 (R2 = 0.30). CSF Aβ1–42, BDNF, α-synuclein, and TPrP changes are evolving in young MCMA urbanites historically showing underperformance in cognitive processes, odor identification deficits, downregulation of frontal cellular PrP, and neuropathological AD and PD hallmarks. Neuroprotection of young MCMA residents ought to be a public health priority.","PeriodicalId":294723,"journal":{"name":"Advances in Alzheimer’s Disease","volume":"103 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124725054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

Particulate Matter Exposure Exacerbates Amyloid-β Plaque Deposition and Gliosis in APP/PS1 Mice 颗粒物质暴露加剧APP/PS1小鼠淀粉样蛋白-β斑块沉积和胶质瘤形成

Advances in Alzheimer’s Disease Pub Date : 1900-01-01 DOI: 10.3233/aiad210013

Bijayani Sahu, A. Mackos, A. Floden, L. Wold, C. Combs

{"title":"Particulate Matter Exposure Exacerbates Amyloid-β Plaque Deposition and Gliosis in APP/PS1 Mice","authors":"Bijayani Sahu, A. Mackos, A. Floden, L. Wold, C. Combs","doi":"10.3233/aiad210013","DOIUrl":"https://doi.org/10.3233/aiad210013","url":null,"abstract":"Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) plaques, neuroinflammation, and neuronal death. There are several well-established genetic and environmental factors hypothesized to contribute to AD progression including air pollution. However, the molecular mechanisms by which air pollution exacerbates AD are unclear. Objective: This study explored the effects of particulate matter exposure on AD-related brain changes using the APP/PS1 transgenic model of disease. Methods: Male C57BL/6;C3H wild type and APP/PS1 mice were exposed to either filtered air (FA) or particulate matter sized under 2.5 μm (PM2.5) for 6 h/day, 5 days/week for 3 months and brains were collected. Immunohistochemistry for Aβ, GFAP, Iba1, and CD68 and western blot analysis for PS1, BACE, APP, GFAP, and Iba1 were performed. Aβ ELISAs and cytokine arrays were performed on frozen hippocampal and cortical lysates, respectively. Results: The Aβ plaque load was significantly increased in the hippocampus of PM2.5-exposed APP/PS1 mice compared to their respective FA controls. Additionally, in the PM2.5-exposed APP/PS1 group, increased astrocytosis and microgliosis were observed as indicated by elevated GFAP, Iba1, and CD68 immunoreactivities. PM2.5 exposure also led to an elevation in the levels of PS1 and BACE in APP/PS1 mice. The cytokines TNF-α, IL-6, IL-1β, IFN-γ, and MIP-3α were also elevated in the cortices of PM2.5-exposed APP/PS1 mice compared to FA controls. Conclusion: Our data suggest that chronic particulate matter exposure exacerbates AD by increasing Aβ plaque load, gliosis, and the brain inflammatory status.","PeriodicalId":294723,"journal":{"name":"Advances in Alzheimer’s Disease","volume":"89 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131343015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Apolipoprotein E4, Gender, Body Mass Index, Inflammation, Insulin Resistance, and Air Pollution Interactions: Recipe for Alzheimer’s Disease Development in Mexico City Young Females 载脂蛋白E4、性别、体重指数、炎症、胰岛素抵抗和空气污染的相互作用:墨西哥城年轻女性阿尔茨海默病发展的处方

Advances in Alzheimer’s Disease Pub Date : 1900-01-01 DOI: 10.3233/aiad210036

L. Calderón-Garcidueñas, S. M. de la Monte

{"title":"Apolipoprotein E4, Gender, Body Mass Index, Inflammation, Insulin Resistance, and Air Pollution Interactions: Recipe for Alzheimer’s Disease Development in Mexico City Young Females","authors":"L. Calderón-Garcidueñas, S. M. de la Monte","doi":"10.3233/aiad210036","DOIUrl":"https://doi.org/10.3233/aiad210036","url":null,"abstract":"Given the epidemiological trends of increasing Alzheimer’s disease (AD) and growing evidence that exposure and lifestyle factors contribute to AD risk and pathogenesis, attention should be paid to variables such as air pollution, in order to reduce rates of cognitive decline and dementia. Exposure to fine particulate matter (PM2.5) and ozone (O3) above the US EPA standards is associated with AD risk. Mexico City children experienced pre- and postnatal high exposures to PM2.5, O3, combustion-derived iron-rich nanoparticles, metals, polycyclic aromatic hydrocarbons, and endotoxins. Exposures are associated with early brain gene imbalance in oxidative stress, inflammation, innate and adaptive immune responses, along with epigenetic changes, accumulation of misfolded proteins, cognitive deficits, and brain structural and metabolic changes. The Apolipoprotein E (APOE) 4 allele, the most prevalent genetic risk for AD, plays a key role in the response to air pollution in young girls. APOE 4 heterozygous females with >75% to <94% BMI percentiles are at the highest risk of severe cognitive deficits (1.5–2 SD from average IQ). This review focused on the relationships between gender, BMI, systemic and neural inflammation, insulin resistance, hyperleptinemia, dyslipidemia, vascular risk factors, and central nervous system involvement in APOE4 urbanites exposed to PM2.5 and magnetite combustion-derived iron-rich nanoparticles that can reach the brain. APOE4 young female heterozygous carriers constitute a high-risk group for a fatal disease: AD. Multidisciplinary intervention strategies could be critical for prevention or amelioration of cognitive deficits and long-term AD progression in young individuals at high risk.","PeriodicalId":294723,"journal":{"name":"Advances in Alzheimer’s Disease","volume":"18 24","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132512014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Environmental Nanoparticles, SARS-CoV-2 Brain Involvement, and Potential Acceleration of Alzheimer’s and Parkinson’s Diseases in Young Urbanites Exposed to Air Pollution 环境纳米颗粒、SARS-CoV-2脑介入以及暴露于空气污染的年轻城市居民阿尔茨海默病和帕金森病的潜在加速

Advances in Alzheimer’s Disease Pub Date : 1900-01-01 DOI: 10.3233/aiad210046

L. Calderón-Garcidueñas, R. Torres-Jardón, Maricela Franco-Lira, R. Kulesza, A. Gónzalez‐Maciel, R. Reynoso-Robles, Rafael Brito-Aguilar, Berenice García-Arreola, Paula Revueltas-Ficachi, Juana Adriana Barrera-Velázquez, G. García-Alonso, Edgar García-Rojas, P. Mukherjee, R. Delgado‐Chávez

{"title":"Environmental Nanoparticles, SARS-CoV-2 Brain Involvement, and Potential Acceleration of Alzheimer’s and Parkinson’s Diseases in Young Urbanites Exposed to Air Pollution","authors":"L. Calderón-Garcidueñas, R. Torres-Jardón, Maricela Franco-Lira, R. Kulesza, A. Gónzalez‐Maciel, R. Reynoso-Robles, Rafael Brito-Aguilar, Berenice García-Arreola, Paula Revueltas-Ficachi, Juana Adriana Barrera-Velázquez, G. García-Alonso, Edgar García-Rojas, P. Mukherjee, R. Delgado‐Chávez","doi":"10.3233/aiad210046","DOIUrl":"https://doi.org/10.3233/aiad210046","url":null,"abstract":"Alzheimer’s and Parkinson’s diseases (AD, PD) have a pediatric and young adult onset in Metropolitan Mexico City (MMC). The SARS-CoV-2 neurotropic RNA virus is triggering neurological complications and deep concern regarding acceleration of neuroinflammatory and neurodegenerative processes already in progress. This review, based on our MMC experience, will discuss two major issues: 1) why residents chronically exposed to air pollution are likely to be more susceptible to SARS-CoV-2 systemic and brain effects and 2) why young people with AD and PD already in progress will accelerate neurodegenerative processes. Secondary mental consequences of social distancing and isolation, fear, financial insecurity, violence, poor health support, and lack of understanding of the complex crisis are expected in MMC residents infected or free of SARS-CoV-2. MMC residents with pre-SARS-CoV-2 accumulation of misfolded proteins diagnostic of AD and PD and metal-rich, magnetic nanoparticles damaging key neural organelles are an ideal host for neurotropic SARS-CoV-2 RNA virus invading the body through the same portals damaged by nanoparticles: nasal olfactory epithelium, the gastrointestinal tract, and the alveolar-capillary portal. We urgently need MMC multicenter retrospective-prospective neurological and psychiatric population follow-up and intervention strategies in place in case of acceleration of neurodegenerative processes, increased risk of suicide, and mental disease worsening. Identification of vulnerable populations and continuous effort to lower air pollution ought to be critical steps.","PeriodicalId":294723,"journal":{"name":"Advances in Alzheimer’s Disease","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130957875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Long-Term Exposure to Ambient Air Pollution and Cognitive Function Among Hispanic/Latino Adults in San Diego, California 加州圣地亚哥西班牙裔/拉丁裔成年人长期暴露于环境空气污染和认知功能

Advances in Alzheimer’s Disease Pub Date : 1900-01-01 DOI: 10.3233/aiad210025

S. Ilango, Kevin A. González, Linda C. Gallo, M. Allison, Jianwen Cai, C. Isasi, H. Hosgood, Priscilla M Vásquez, D. Zeng, M. Mortamais, H. González, T. Benmarhnia

{"title":"Long-Term Exposure to Ambient Air Pollution and Cognitive Function Among Hispanic/Latino Adults in San Diego, California","authors":"S. Ilango, Kevin A. González, Linda C. Gallo, M. Allison, Jianwen Cai, C. Isasi, H. Hosgood, Priscilla M Vásquez, D. Zeng, M. Mortamais, H. González, T. Benmarhnia","doi":"10.3233/aiad210025","DOIUrl":"https://doi.org/10.3233/aiad210025","url":null,"abstract":"Background: Hispanics/Latinos in the United States are more likely to live in neighborhoods with greater exposure to air pollution and are projected to have the largest increase in dementia among race/ethnic minority groups. Objective: We examined the associations of air pollution with performance on cognitive function tests in Hispanic/Latino adults. Methods: We used data from the San Diego site of the Hispanic Community Health Study/Study of Latinos, an ongoing cohort of Hispanics/Latinos. This analysis focused on individuals ≥45 years of age who completed a neurocognitive battery examining overall mental status, verbal learning, memory, verbal fluency, and executive function (n = 2,089). Air pollution (PM2.5 and O3) before study baseline was assigned to participants’ zip code. Logistic and linear regression were used to estimate the associations of air pollution on overall mental status and domain-specific standardized test scores. Models accounted for complex survey design, demographic, and socioeconomic characteristics. Results: We found that for every 10 μg/m3 increase in PM2.5, verbal fluency worsened (β: −0.21 [95% CI: −0.68, 0.25]). For every 10 ppb increase in O3, verbal fluency and executive function worsened (β: −0.19 [95% CI: −0.34, −0.03]; β: −0.01 [95% CI: −0.01, 0.09], respectively). We did not identify any detrimental effect of pollutants on other domains. Conclusion: Although we found suggestions that air pollution may impact verbal fluency and executive function, we observed no consistent or precise evidence to suggest an adverse impact of air pollution on cognitive level among this cohort of Hispanic/Latino adults.","PeriodicalId":294723,"journal":{"name":"Advances in Alzheimer’s Disease","volume":"425 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124223969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Long-Term Exposure to PM10 and in vivo Alzheimer’s Disease Pathologies 长期暴露于PM10与体内阿尔茨海默病病理

Advances in Alzheimer’s Disease Pub Date : 1900-01-01 DOI: 10.3233/aiad210012

Jun Ho Lee, M. Byun, D. Yi, K. Ko, S. Jeon, B. Sohn, Jun-Young Lee, Younghwan Lee, Haejung Joung, D. Y. Lee

{"title":"Long-Term Exposure to PM10 and in vivo Alzheimer’s Disease Pathologies","authors":"Jun Ho Lee, M. Byun, D. Yi, K. Ko, S. Jeon, B. Sohn, Jun-Young Lee, Younghwan Lee, Haejung Joung, D. Y. Lee","doi":"10.3233/aiad210012","DOIUrl":"https://doi.org/10.3233/aiad210012","url":null,"abstract":"Background: Previous studies indicated an association between Alzheimer’s disease (AD) dementia and air particulate matter (PM) with aerodynamic diameter <10 μm (PM10), as well as smaller PM. Limited information, however, is available for the neuropathological links underlying such association. Objective: This study aimed to investigate the relationship between long-term PM10 exposure and in vivo pathologies of AD using multimodal neuroimaging. Methods: The study population consisted of 309 older adults without dementia (191 cognitively normal and 118 mild cognitive impairment individuals), who lived in Republic of Korea. Participants underwent comprehensive clinical assessments, 11C-Pittsburg compound B (PiB) positron emission tomography (PET), and magnetic resonance imaging scans. A subset of 78 participants also underwent 18F-AV-1451 tau PET evaluation. The mean concentration of PM with aerodynamic diameter <10 μm over the past 5 years (PM10mean) collected from air pollution surveillance stations were matched to each participant’s residence. Results: In this non-demented study population, of which 62% were cognitively normal and 38% were in mild cognitive impairment state, exposure to the highest tertile of PM10mean was associated with increased risk of amyloid-β (Aβ) positivity (odds ratio 2.19, 95% confidence interval 1.13 to 4.26) even after controlling all potential confounders. In contrast, there was no significant associations between PM10mean exposure and tau accumulation. AD signature cortical thickness and white matter hyperintensity volume were also not associated with PM10mean exposure. Conclusion: The findings suggest that long-term exposure to PM10 may contribute to pathological Aβ deposition.","PeriodicalId":294723,"journal":{"name":"Advances in Alzheimer’s Disease","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130952826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Air Pollution Neurotoxicity in the Adult Brain: Emerging Concepts from Experimental Findings 空气污染:成人大脑中的神经毒性:来自实验发现的新概念

Advances in Alzheimer’s Disease Pub Date : 1900-01-01 DOI: 10.3233/aiad210045

A. Haghani, T. Morgan, H. Forman, C. Finch

{"title":"Air Pollution Neurotoxicity in the Adult Brain: Emerging Concepts from Experimental Findings","authors":"A. Haghani, T. Morgan, H. Forman, C. Finch","doi":"10.3233/aiad210045","DOIUrl":"https://doi.org/10.3233/aiad210045","url":null,"abstract":"Epidemiological studies are associating elevated exposure to air pollution with increased risk of Alzheimer’s disease and other neurodegenerative disorders. In effect, air pollution accelerates many aging conditions that promote cognitive declines of aging. The underlying mechanisms and scale of effects remain largely unknown due to its chemical and physical complexity. Moreover, individual responses to air pollution are shaped by an intricate interface of pollutant mixture with the biological features of the exposed individual such as age, sex, genetic background, underlying diseases, and nutrition, but also other environmental factors including exposure to cigarette smoke. Resolving this complex manifold requires more detailed environmental and lifestyle data on diverse populations, and a systematic experimental approach. Our review aims to summarize the modest existing literature on experimental studies on air pollution neurotoxicity for adult rodents and identify key gaps and emerging challenges as we go forward. It is timely for experimental biologists to critically understand prior findings and develop innovative approaches to this urgent global problem. We hope to increase recognition of the importance of air pollution on brain aging by our colleagues in the neurosciences and in biomedical gerontology, and to support the immediate translation of the findings into public health guidelines for the regulation of remedial environmental factors that accelerate aging processes.","PeriodicalId":294723,"journal":{"name":"Advances in Alzheimer’s Disease","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129174770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0