RESUMEN
Research on the impact of diet and memory has garnered considerable attention while exploring the link between obesity and cognitive impairment. High-fat diet (HFD) rodent models recapitulate the obesity phenotype and subsequent cognitive impairments. While it is known that HFD is associated with sensory impairment, little attention has been given to the potential role these sensory deficits may play in recognition memory testing, one of the most commonly used cognitive tests. Because mice utilize their facial whiskers as their primary sensory apparatus, we modified a common recognition test, the novel object recognition task, by replacing objects with sandpaper grits at ground level, herein referred to as the novel tactile recognition task (NTR). First, we tested whisker-manipulated mice in this task to determine its reliance on intact whiskers. Then, we tested the HFD mouse in the NTR. Finally, to ensure that deficits in the NTR are due to cognitive impairment and not HFD-induced sensory deficiencies, we tested the whisker sensitivity of HFD mice via the corner test. Our results indicate that the NTR is a whisker dependent task, and that HFD mice exhibit tactile recognition memory impairment, not accompanied by whisker sensory deficits.
Asunto(s)
Dieta Alta en Grasa , Discriminación en Psicología , Memoria , Reconocimiento en Psicología , Tacto , Animales , Conducta Animal , Disfunción Cognitiva/etiología , Masculino , Ratones Endogámicos C57BL , Estimulación Física , Percepción del Tacto , VibrisasRESUMEN
In order for Alzheimer's disease (AD) to manifest, cells must communicate "pathogenic material" such as proteins, signaling molecules, or genetic material to ensue disease propagation. Small extracellular vesicles are produced via the endocytic pathways and released by nearly all cell types, including neurons. Due to their intrinsic interrelationship with endocytic processes and autophagy, there has been increased interest in studying the role of these neuronally-derived extracellular vesicles (NDEVs) in the propagation of AD. Pathologic cargo associated with AD have been found in a number of studies, and NDEVs have been shown to induce pathogenesis in vivo and in vitro. Exogenous NDEVs are also shown to reduce plaque burden in AD models. Thus, the NDEV has the potential to become a useful biomarker, a pathologic potentiator, and a therapeutic opportunity. While the field of NDEV research in AD is still in its infancy, we review the current literature supporting these three claims.