The protective effect of early dietary fat consumption on Alzheimer's disease–related pathology and cognitive function in mice

• Published in: Alzheimer's & dementia : translational research & clinical interventions Vol. 7; no. 1; pp. e12173 - n/a
• Main Authors: Amelianchik, Anna, Merkel, Jonathan, Palanisamy, Premkumar, Kaneki, Shigeru, Hyatt, Emily, Norris, Erin H.
• Format: Journal Article
• Language: English
• Published: United States John Wiley & Sons, Inc 2021; John Wiley and Sons Inc; Wiley
• Subjects: Alzheimer's disease; amyloid beta; Animal cognition; Blood-brain barrier; Body composition; Body mass index; Brain research; Carbohydrates; Cholesterol; Cognitive ability; Dementia; Diabetes; Diet; fibrinogen; Glucose; high‐fat diet; Laboratory animals; Obesity; Oils & fats; Pathology; Plasma; Proteins; Statistical analysis; Systematic review; Variance analysis; Weight control; high‐fat diet; fibrinogen; Alzheimer's disease; amyloid beta; obesity
• ISSN: 2352-8737; 2352-8737
• DOI: 10.1002/trc2.12173

Introduction It has been suggested that obesity may influence Alzheimer's disease (AD) pathogenesis, yet the numerous publications on this topic have inconsistent results and conclusions. Methods Our study examined the effect of varying the timing of high‐fat diet (HFD) consumption on AD‐related pathology and cognition in transgenic Tg6799 AD mice. Results HFD feeding starting at or before 3 months of age, prior to severe AD pathology, had protective effects in AD mice: reduced extracellular amyloid beta (Aβ) deposition, decreased fibrinogen extravasation into the brain parenchyma, and improved cognitive function. However, delaying HFD consumption until 6 months of age, when AD pathology is ubiquitous, reduced these protective effects in AD mice. Discussion Overall, we demonstrate that the timeline of HFD consumption may play an important role in how dietary fats affect AD pathogenesis and cognitive function.