Cross Talk Between Brain Innate Immunity and Serotonin Signaling Underlies Depressive-Like Behavior Induced by Alzheimer's Amyloid-β Oligomers in Mice.
Jose Henrique LedoEstefania P AzevedoDanielle BeckmanFelipe C RibeiroLuís Eduardo SantosDaniela Soares RazolliGrasielle C KincheskiHelen M MeloMaria BellioAntonio L TeixeiraLicio Augusto VellosoDebora FoguelFernanda G De FeliceSergio T FerreiraPublished in: The Journal of neuroscience : the official journal of the Society for Neuroscience (2017)
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the main cause of dementia in the world. Brain accumulation of amyloid-β oligomers (AβOs) is a major feature in the pathogenesis of AD. Although clinical and epidemiological data suggest a strong connection between AD and depression, the underlying mechanisms linking these two disorders remain largely unknown. Here, we report that aberrant activation of the brain innate immunity and decreased serotonergic tonus in the brain are key players in AβO-induced depressive-like behavior in mice. Our findings may open up new possibilities for the development of effective therapeutics for AD and depression aimed at modulating microglial function.
Keyphrases
- resting state
- white matter
- functional connectivity
- cognitive decline
- depressive symptoms
- cerebral ischemia
- bipolar disorder
- mild cognitive impairment
- spinal cord injury
- type diabetes
- sleep quality
- signaling pathway
- deep learning
- oxidative stress
- electronic health record
- lipopolysaccharide induced
- cognitive impairment
- physical activity
- lps induced
- blood brain barrier
- subarachnoid hemorrhage
- brain injury