マイクロプラスチック曝露がマウスのアルツハイマー病を引き起こす可能性(URI study links microplastic exposure to Alzheimer’s disease in mice)

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2025-09-10 ロードアイランド大学(URI)

ロードアイランド大学の研究チームは、マイクロプラスチック曝露がアルツハイマー病リスクを高める可能性をマウス実験で確認した。APOE4遺伝子を持つマウスに3週間ポリスチレン粒子を混ぜた水を与えると、粒子は血液脳関門を通過して脳に蓄積した。行動試験では雄で活動低下や無気力、雌で記憶課題の成績低下が見られ、人のアルツハイマー病に見られる性差と一致した。これは遺伝要因と環境要因が複合して神経変性を進行させることを示唆している。研究は、マイクロプラスチックが単なる環境問題にとどまらず、神経疾患リスク因子となる可能性を示し、予防策や規制強化の必要性を訴えている。成果は環境毒性と神経科学を結ぶ重要な知見として注目されている。

<関連情報>

ポリスチレン微小プラスチックへの短期曝露は、アポリポプロテインE(APOE)遺伝子型および性別に依存した認知機能・免疫・代謝マーカーを変化させる Short-term exposure to polystyrene microplastics alters cognition, immune, and metabolic markers in an apolipoprotein E (APOE) genotype and sex-dependent manner

Lauren Gaspar, Sydney Bartman, Hannah Tobias-Wallingford, Giuseppe Coppotelli and Jaime M Ross
Environmental Research Communications  Published: 20 August 2025
DOI:10.1088/2515-7620/adf8ae

マイクロプラスチック曝露がマウスのアルツハイマー病を引き起こす可能性(URI study links microplastic exposure to Alzheimer’s disease in mice)

Abstract

Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders and one of the leading causes of death in individuals over the age of 65. Most cases of AD develop sporadically, however, there are several risk factors that have been identified which significantly increases an individual’s risk for developing AD. The most prominent of these is Apolipoprotein E4 (APOE4), which can potentially result in an up to 10-fold greater risk of developing AD. The presence of APOE4 alone, however, cannot be solely responsible for AD as the disease may occur even in the absence of APOE4. Therefore, there must be other contributing factors such as exposure to environmental toxins including heavy metals and pesticides, which have independently been shown to contribute to AD. Nano- and microplastics (NMPs) are plastic particles less than 1 μm and 5 mm in size, respectively, and have only recently been identified as a major environmental pollutant with serious health concerns. Given the adverse health effects that are increasingly being associated with NMPs exposure, we sought to understand how the combination of APOE4 and NMPs exposure may work synergistically to promote cognitive dysfunction and alter key regulatory pathways to impact overall health. Following a short-term (3 week) exposure to pristine spherical fluorescently-labeled 0.1 and 2 μm polystyrene (PS) NMPs, we found significant sex-dependent alterations in locomotor and recognition memory in APOE4 mice, but not in APOE3 controls. We additionally found that exposure to PS-NMPs resulted in sex and genotype specific alterations in astrocytic and microglial markers in the brain, and in CYP1A1, a major metabolizer of environmental polycyclic aromatic hydrocarbons, in the liver. These results suggest PS-NMPs may interact with the APOE4 allele to promote cognitive dysfunction and alter immune and metabolic pathways which may contribute to disease-like states.

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