Journal of toxicology · 2025
Impact of Particulate Matter 2.5 on Neurological Diseases: Insights Into Pathophysiological and Molecular Mechanisms.
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Rubio Carmen, López-Landa Alejandro, Serrano-García Norma, Romo-Parra Héctor, Rubio-Osornio Moisés
Аннотация
BACKGROUND: Fine particulate matter (PM2.5) has been significantly linked to the progression of various neurological and neurodegenerative diseases.
OBJECTIVE: This review aims to elucidate the molecular and pathophysiological effects induced by chronic exposure to PM2.5 in neurological and neurodegenerative diseases, including Alzheimer's, Parkinson's, Huntington's, multiple sclerosis, and epilepsy.
INTRODUCTION: PM2.5 penetrates the central nervous system (CNS) via the olfactory nerve or by disrupting the blood-brain barrier (BBB), triggering oxidative stress, neuroinflammation, mitochondrial dysfunction, and epigenetic alterations.
DISCUSSION: In Alzheimer's and Parkinson's diseases, PM2.5 exacerbates the accumulation of β-amyloid, hyperphosphorylated tau, and α-synuclein, while in Huntington's disease, it worsens toxicity mediated by mutant huntingtin. In multiple sclerosis, these particles intensify neuroinflammation and axonal damage, whereas in epilepsy, they promote neuronal hyperexcitability and recurrent seizures. These mechanisms contribute to neuronal damage, symptom progression, and functional decline.
CONCLUSION: This evidence highlights the urgent need for strict environmental policies to reduce PM2.5 exposure and further research to develop therapeutic strategies that mitigate its effects on neurological diseases, thereby improving the health of vulnerable populations.
OBJECTIVE: This review aims to elucidate the molecular and pathophysiological effects induced by chronic exposure to PM2.5 in neurological and neurodegenerative diseases, including Alzheimer's, Parkinson's, Huntington's, multiple sclerosis, and epilepsy.
INTRODUCTION: PM2.5 penetrates the central nervous system (CNS) via the olfactory nerve or by disrupting the blood-brain barrier (BBB), triggering oxidative stress, neuroinflammation, mitochondrial dysfunction, and epigenetic alterations.
DISCUSSION: In Alzheimer's and Parkinson's diseases, PM2.5 exacerbates the accumulation of β-amyloid, hyperphosphorylated tau, and α-synuclein, while in Huntington's disease, it worsens toxicity mediated by mutant huntingtin. In multiple sclerosis, these particles intensify neuroinflammation and axonal damage, whereas in epilepsy, they promote neuronal hyperexcitability and recurrent seizures. These mechanisms contribute to neuronal damage, symptom progression, and functional decline.
CONCLUSION: This evidence highlights the urgent need for strict environmental policies to reduce PM2.5 exposure and further research to develop therapeutic strategies that mitigate its effects on neurological diseases, thereby improving the health of vulnerable populations.