Artikel ; Online: Early Life Obesity Increases Neuroinflammation, Amyloid Beta Deposition, and Cognitive Decline in a Mouse Model of Alzheimer's Disease.
2023 Band 15, Heft 11
Abstract: Obesity, a known risk factor of Alzheimer's disease (AD), increases the activation of microglia, leading to a proinflammatory phenotype. Our previous work shows that a high fat diet (HFD) can cause neuroinflammation and cognitive decline in mice. We ... ...
Abstract | Obesity, a known risk factor of Alzheimer's disease (AD), increases the activation of microglia, leading to a proinflammatory phenotype. Our previous work shows that a high fat diet (HFD) can cause neuroinflammation and cognitive decline in mice. We hypothesized that proinflammatory activation of brain microglia in obesity exacerbates AD pathology and increases the accumulation of amyloid beta (Aβ) plaques. Presently, we tested cognitive function in 8-month-old male and female APP/PS1 mice fed a HFD, starting at 1.5 months of age. Locomotor activity, anxiety-like behavior, behavioral despair, and spatial memory were all assessed through behavioral tests. Microgliosis and Aβ deposition were measured in multiple brain regions through immunohistochemical analysis. Our results show that a HFD decreases locomotor activity, while increasing anxiety-like behavior and behavioral despair independent of genotype. A HFD led to increased memory deficits in both sexes, with HFD-fed APP/PS1 mice performing the worst out of all groups. Immunohistochemical analysis showed increased microgliosis in mice fed a HFD. This was accompanied by an increase in Aβ deposition in the HFD-fed APP/PS1 mice. Together, our results support that HFD-induced obesity exacerbates neuroinflammation and Aβ deposition in a young adult AD mouse model, leading to increased memory deficits and cognitive decline in both sexes. |
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Mesh-Begriff(e) | Male ; Mice ; Female ; Animals ; Alzheimer Disease/genetics ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Neuroinflammatory Diseases ; Mice, Transgenic ; Memory Disorders/complications ; Cognitive Dysfunction/complications ; Disease Models, Animal ; Plaque, Amyloid/genetics ; Obesity/complications ; Presenilin-1/genetics |
Chemische Substanzen | Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Presenilin-1 |
Sprache | Englisch |
Erscheinungsdatum | 2023-05-27 |
Erscheinungsland | Switzerland |
Dokumenttyp | Journal Article |
ZDB-ID | 2518386-2 |
ISSN | 2072-6643 ; 2072-6643 |
ISSN (online) | 2072-6643 |
ISSN | 2072-6643 |
DOI | 10.3390/nu15112494 |
Datenquelle | MEDical Literature Analysis and Retrieval System OnLINE |
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