Pre-symptomatic synaptic dysfunction and longitudinal decay of hippocampal synaptic function in APPPS1 mouse model of Alzheimer's disease is sex-independent.

Alzheimer's disease (AD) is an incurable, age-related and progressive neurodegenerative disease characterized by cognitive impairments. Deficits in synaptic plasticity were reported in various models of AD-like pathology and are considered as an early contributing factor of cognitive impairment. However, the majority of previous studies were focused on overt, symptomatic stages of pathology and assessed long-term potentiation (LTP), whereas long-term depression (LTD) was much less investigated and the precise nature of its involvement remains poorly defined.

Dysfunction of the glutamatergic photoreceptor synapse in the P301S mouse model of tauopathy.

Tauopathies, including Alzheimer's disease, are characterized by retinal ganglion cell loss associated with amyloid and phosphorylated tau deposits. We investigated the functional impact of these histopathological alterations in the murine P301S model of tauopathy. Visual impairments were demonstrated by a decrease in visual acuity already detectable at 6 months, the onset of disease.

Neuroinflammation: A Possible Link Between Chronic Vascular Disorders and Neurodegenerative Diseases.

Various age-related diseases involve systemic inflammation, i.e. a stereotyped series of acute immune system responses, and aging itself is commonly associated with low-grade inflammation or inflamm'aging.

Concomitant Retinal Alterations in Neuronal Activity and TNFα Pathway Are Detectable during the Pre-Symptomatic Stage in a Mouse Model of Alzheimer's Disease.

The pre-symptomatic stage of Alzheimer's disease (AD) is associated with increased amyloid-β (Aβ) precursor protein (APP) processing and Aβ accumulation in the retina and hippocampus. Because neuronal dysfunctions are among the earliest AD-related alterations, we asked whether they are already detectable in the retina during the pre-symptomatic stage in a APPswePS1dE9 (APP/PS1) mouse model. The age chosen for the study (3-4 months) corresponds to the pre-symptomatic stage because no retinal Aβ was detected, in spite of the presence of βCTF (the first cleavage product of APP).

Microbiota in neuroinflammation and synaptic dysfunction: a focus on Alzheimer's disease.

Background: The implication of gut microbiota in the control of brain functions in health and disease is a novel, currently emerging concept. Accumulating data suggest that the gut microbiota exert its action at least in part by modulating neuroinflammation. Given the link between neuroinflammatory changes and neuronal activity, it is plausible that gut microbiota may affect neuronal functions indirectly by impacting microglia, a key player in neuroinflammation.