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Traffic noise exposure, cognitive decline, and amyloid‐beta pathology in an AD mouse model
Author(s) -
Karem Hadil,
Mehla Jogender,
Kolb Bryan E.,
Mohajerani Majid H.
Publication year - 2021
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.22192
Subject(s) - cognition , medicine , endocrinology , anxiety , dementia , corticosterone , cognitive decline , amyloid beta , oxidative stress , effects of sleep deprivation on cognitive performance , disease , neuroscience , pathology , psychology , physiology , hormone , psychiatry
Concerns are growing that exposure to environmental pollutants, such as traffic noise, might cause cognitive impairments and predispose individuals toward the development of Alzheimer's disease (AD) dementia. In this study in a knock‐in mouse model of AD, we investigated how chronic traffic noise exposure (CTNE) impacts cognitive performance and amyloid‐beta (Aβ) pathology. A group of APP NL‐G‐F/NL‐G‐F mice was exposed to CTNE (70 dB A , 8 hr/day for 1 month) and compared with nonexposed counterparts. Following CTNE, an increase in hypothalamic–pituitary–adrenal (HPA) axis responsivity was observed by corticosterone assay of the blood. One month after CTNE, the CTNE group demonstrated impairments in cognitive and motor functions, and indications of anxiety‐like behavior, relative to the control animals. The noise‐exposed group also showed elevated Aβ aggregation, as inferred by a greater number of plaques and larger average plaque size in various regions of the brain, including regions involved in stress regulation. The results support that noise‐associated dysregulation of the neuroendocrine system as a potential risk factor for developing cognitive impairment and Aβ pathology, which should be further investigated in human studies.