scispace - formally typeset
Search or ask a question

Are there any epidemiological studies in the last five years linking air pollution exposure to alzheimer's disease? 

Interquartile range
Inhalation
Inhalation exposure
Biomarker
Cognitive decline
Best insight from top research papers

Recent epidemiological studies have indeed linked air pollution exposure to Alzheimer's disease. Studies have shown that exposure to fine particulate matter (PM2.5) from ambient and traffic-related sources is associated with adverse effects on cognition and an increased risk of Alzheimer's disease, as indicated by changes in cerebrospinal fluid biomarkers related to the disease . Furthermore, research on inhalation exposure to traffic-related air pollution has demonstrated an acceleration in amyloid-β plaque formation, a hallmark of Alzheimer's disease, in animal models . Additionally, a systematic review and meta-analysis of population-based cohort studies revealed a significant association between air pollution exposure and dementia risk, with specific pollutants like PM2.5, PM10, carbon monoxide, nitrogen dioxide, and nitrogen oxides showing increased risk, emphasizing the importance of controlling air pollution to reduce dementia globally .

Answers from top 5 papers

More filters
Papers (5)Insight
Open access•Journal Article•DOI
Air pollution is associated with faster cognitive decline in Alzheimer's disease
Younggun Lee, Seon Jin Yoon, So Hoon Yoon, Seun Jeon, Minseok Kim, Dong Ah Shin, Chung Mo Nam, Byoung Seok Ye 
27 Apr 2023-Annals of clinical and translational neurology
Yes, recent research suggests that chronic exposure to air pollution is linked to faster cognitive decline in Alzheimer's disease, indicating an epidemiological association between air pollution and Alzheimer's disease progression.
Journal Article•DOI
98 Inhalation Exposure to Traffic-Related Air Pollution Accelerates Alzheimer’s Disease-like Pathology in a Murine Model
Tina Wahle, Adriana Sofranko, Eleonora Scarcello, Isabelle Masson, Catrin Albrecht, Gerrit Bredeck, Mathias Busch, Paul H. B. Fokkens, John Boere, Flemming R. Cassee, Roel P. F. Schins 
01 May 2023-Annals of Work Exposures and Health
Yes, recent epidemiological studies have linked exposure to traffic-related air pollution to Alzheimer's disease, as shown in the study "Inhalation Exposure to Traffic-Related Air Pollution Accelerates Alzheimer’s Disease-like Pathology."
Open access•Journal Article•DOI
Association of air pollution with dementia: a systematic review with meta-analysis including new cohort data from China
Ilma Ainayatu Ahlin
01 Apr 2023-Environmental research
Yes, recent epidemiological studies, including one in China, link air pollution exposure to Alzheimer's disease, showing a significantly increased risk (RR 2.28) with higher air quality index (AQI).
Open access•Posted Content•DOI
Association between Fine Particulate Matter Exposure and Cerebrospinal Fluid Biomarkers of Alzheimer's Disease among a Cognitively Healthy Population-based Cohort
Evelyn Casey, Z. Li, Danyan Liang, Stefanie T. Ebelt, A. Levey, J. Lah, T. Wingo, A. Huels 
20 Jun 2023-medRxiv
Yes, recent epidemiological research found a negative association between fine particulate matter (PM2.5) exposure and Alzheimer's disease biomarkers, indicating a potential link between air pollution and Alzheimer's disease.
Journal Article•DOI
The role of environmental air pollution in the development of alzheimer’s disease
M.I. Beriashvili, Gigi Gorgadze 
07 Jun 2023-JUNIOR RESEARCHERS
Yes, recent studies have linked air pollution exposure to Alzheimer's disease, suggesting a potential role in its development through oxidative stress, neuroinflammation, and neurodegenerative changes.

See what other people are reading

Who is the author of the cognitive effect of vape?
5 answers
The author of the study on the cognitive effects of vaping is Arwa Ali S. Al-Mshari, Mona H. AlSheikh, Rabia Latif, and Sadaf Mumtaz. The research conducted by these authors aimed to establish an association between cigarette smoking, cognition, and plasma brain-derived neurotrophic factor (BDNF) levels in healthy young adults. The study involved assessing cognitive function using the Cambridge Neuropsychological Test Automated Battery (CANTAB) and measuring plasma BDNF levels in healthy male participants, both smokers and non-smokers. The results indicated that young smokers exhibited impaired sustained attention and reduced ability to manage conflicting information compared to non-smokers. Additionally, a positive correlation was found between plasma BDNF levels and the number of cigarettes smoked per day.Isoforms of the protein clusterin
4 answers
Clusterin (CLU) has multiple isoforms with distinct functions. In Alzheimer's disease, a non-glycosylated 45 kDa isoform called mitoCLU is found in the mitochondrial matrix of neurons and astrocytes, contributing to disease development. In osteoarthritis, two isoforms of clusterin have opposing roles: secreted clusterin (sCLU) acts as a cytoprotective chaperone, while nuclear clusterin (nCLU) promotes cell death. Additionally, CLU isoforms play a role in oral squamous cell carcinoma (OSCC), where abnormal expression is linked to cancer progression, but the exact roles in carcinogenesis remain unclear. The presence of sCLU and nCLU isoforms has also been observed in a primary culture of porcine aortic endothelial cells, with sCLU being the predominant form influenced by lipopolysaccharide exposure.How long does acl rehabilitaion take for returning to sport?
5 answers
Return to sport (RTS) after anterior cruciate ligament reconstruction (ACLR) typically takes around 9 months, as suggested by current timelines. Prehabilitation before ACLR, lasting 4-6 weeks, can enhance early to mid-term strength and motion, improving the chances of a successful return to sport. Revision ACLR outcomes show that almost 40% of patients return to their preinjury sports level, with 60% returning at a lower level, emphasizing the variability in return to sport rates after revision surgery. A survey of orthopedic surgeons revealed that RTS criteria after primary ACLR vary, with RTS occurring sooner in non-pivoting sports compared to pivoting sports, typically between 5-10 months post-surgery, with psychological readiness often not assessed. Different rehabilitation approaches exist, with a conservative model aiming for RTS at 9 months or later, while an accelerated approach targets a return to sport by 6 months.How does bed positioning affect the severity of obstructive sleep apnea (OSA)?
5 answers
Bed positioning plays a crucial role in affecting the severity of obstructive sleep apnea (OSA). Studies have shown that positional obstructive sleep apnea (POSA) is prevalent in both adultsand children. Positional therapy (PT) in non-supine sleeping positions has been found to significantly reduce OSA severity, making it a viable low-cost and non-invasive intervention. Additionally, the use of intelligent sleep apnea beds (ISABel) has been explored, showing that tilting beds can potentially reduce supine AHI and prolong the time to the next apnea/hypopnea event. Furthermore, in severe cases of positional obstructive sleep apnea syndrome (POSAS), mandibular advancement devices (MADs) have been effective in reducing AHI and improving quality of life, serving as an alternative to CPAP therapy.What is the need of blood biomarkers of TBI?
4 answers
Blood biomarkers of Traumatic Brain Injury (TBI) are crucial for accurate diagnosis and prognosis assessment. These biomarkers, such as S100B, GFAP, UCHL1, NF-L, and tau, provide insights into the severity of TBI, staging within the injury and recovery processes, and quantifiable metrics for brain injury reversal and recovery. They help in predicting TBI, post-traumatic stress disorder (PTSD), and chronic traumatic encephalopathy (CTE) by quantifying specific protein structures and properties. Blood-based biomarkers aid in diagnosing TBI across different age groups, with potential to streamline diagnosis, especially in older adults. Additionally, these biomarkers can reduce unnecessary transfers for MRI scans in critically ill TBI patients, enhancing patient management without added costs. The development of blood biomarkers, along with biosensing techniques, offers a rapid, sensitive, and cost-effective approach for early TBI detection and improved treatment strategies.Is gastrografin absorbed from the peritoneum?
5 answers
Gastrografin can be absorbed from the peritoneum, as evidenced by studies. Research on rabbits showed that after intraperitoneal injection, gastrografin was rapidly absorbed, contrasting with barium sulfate which remained in the abdominal area. Dual-energy CT scans successfully detected and quantified gastrografin in ex vivo samples, stool specimens, and biological solutions, indicating its absorption and stability over time. Additionally, a study on newborn rats revealed that gastrografin caused severe damage to the small intestine mucosa, leading to translocation of bacteria into the peritoneal cavity, further supporting its absorption and detrimental effects. Therefore, the evidence suggests that gastrografin can indeed be absorbed from the peritoneum.Does the cost of hospitalisation vary by Race and ethnicity in Australia?
5 answers
The cost of hospitalization in Australia varies by race and ethnicity. Studies show that Aboriginal Australians experience higher costs for potentially preventable hospitalizations (PPH) compared to non-Aboriginal individuals, with increased costs associated with higher levels of disadvantage and remoteness. Additionally, culturally and linguistically diverse (CALD) patients tend to incur higher healthcare costs due to a higher burden of disease and increased resource consumption. Furthermore, while Indigenous youth have higher rates of hospitalised self-harm, the cost per episode is lower compared to non-Indigenous youth. Moreover, Aboriginal patients with ischemic heart disease (IHD) incur lower total costs per person compared to non-Aboriginal patients, particularly in specific comorbidities like diabetes and chronic kidney disease. These findings underscore the impact of race and ethnicity on healthcare costs in Australia.How does a high sugar diet impact DNA methylation patterns in humans?
5 answers
A high sugar diet can significantly impact DNA methylation patterns in humans. Research indicates that high glucose levels, as seen in prediabetic conditions, can cause epigenetic changes in pancreatic beta cells, potentially contributing to diabetes etiology. Maternal consumption of added sugar during pregnancy is associated with altered placental DNA methylation and reduced fetal movement, affecting offspring health. Moreover, exposure to high glucose levels can lead to gene-specific DNA methylation alterations in human neural progenitor cells, affecting pathways crucial for neurodevelopment. Additionally, high dietary glycemic index and load are negatively associated with global DNA methylation levels, suggesting that carbohydrate intake influences DNA methylation patterns in an Italian population. These findings collectively highlight the significant impact of a high sugar diet on DNA methylation patterns, potentially influencing various aspects of health and development in humans.How does the mechanism of cell competition contribute to the aging process in basal keratinocytes?
5 answers
The mechanism of cell competition contributes to the aging process in basal keratinocytes through fluctuations in the expression of specific proteins like collagen XVII (COL17A1). This fluctuation, induced by genomic/oxidative stress, leads to differential expression levels of COL17A1 among individual stem cells, creating a driving force for cell competition. Clones expressing high levels of COL17A1 outcompete and eliminate adjacent stressed clones with low COL17A1 expression, ultimately affecting tissue homeostasis and aging. The loss of COL17A1 in high-potential stem cells limits their competitive ability, contributing to skin aging by causing hemidesmosome fragility and stem cell delamination, depleting neighboring cells and promoting skin aging. This process highlights potential therapeutic targets for anti-aging interventions in basal keratinocytes.What are the potential mechanisms underlying the association between ICIP and TMB, and how might these influence treatment decisions?
5 answers
The association between immune checkpoint inhibitor therapy (ICI) and tumor mutational burden (TMB) involves several key mechanisms. High TMB has been linked to improved survival with ICI treatment, but not all high-TMB patients respond well. Specific gene alterations impact outcomes differently in TMB-high and TMB-low patients, influencing response to ICI. For instance, mutations in genes like STK11 and E2F3 are associated with worse outcomes in TMB-high tumors, while mutations in genes like NTRK and PTPRD are linked to better outcomes. Additionally, the immune-excluded phenotype, characterized by high stromal TIL and low intratumoral TIL density, is correlated with high TGFBs and poor response to immunotherapy. These insights can guide treatment decisions by helping identify patients likely to benefit from ICI based on their TMB status and specific gene alterations.How does the expression of p16 vary across different types of epidermal tissues?
5 answers
The expression of p16 varies across different types of epidermal tissues. In seborrheic keratosis (SK), p16 protein expression differs between single and multiple lesions, with single SK patients showing negative-weak expression and multiple SK patients exhibiting moderate-strong expression. In Bowen disease (BD) and benign seborrheic keratosis (SK), p16 expression patterns also differ, with p16 being positive in BD and negative in SK, while clonal seborrheic keratosis (CSK) shows varying levels of p16 positivity in clonal nests. Additionally, p16 expression in Merkel cell carcinoma (MCC) and inflammatory skin diseases like lichen planus, graft-versus-host disease, and psoriasis is associated with cellular senescence and upregulated by aging stimuli, indicating a role in the pathogenesis of these conditions.