Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease

Abstract

Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hippocampus is specifically associated with major hippocampal excitatory pathways and is related to neuronal calcium regulation. Here, we investigated the hippocampal expression of brain‐specific neuroplastin isoform (Np65), its relationship with amyloid and tau pathology in Alzheimer's disease (AD), and potential involvement of neuroplastin in tissue response during the disease progression. Np65 expression and localization was analysed in six human hippocampi with confirmed AD neuropathology, and six age‐/gender‐matched control hippocampi by imunohistochemistry. In AD cases with shorter disease duration, the Np65 immunoreactivity was significantly increased in the dentate gyrus (DG), Cornu Ammonis 2/3 (CA2/3), and subiculum, with the highest level of Np expression being located on the dendrites of granule cells and subicular pyramidal neurons. Changes in the expression of neuroplastin in AD hippocampal areas seem to be related to the progression of disease. Our study suggests that cell‐adhesion protein neuroplastin is involved in tissue reorganization and is a potential molecular marker of plasticity response in the early neurodegeneration process of AD.

The innate immune toll-like-receptor-2 modulates the depressogenic and anorexiolytic neuroinflammatory response in obstructive sleep apnoea

“…long-term potentiation), formation and a balance of the excitatory/inhibitory synapses 47 , in shaping of brain's cortical thickness 48 . Moreover, its involvement in early tissue response in hippocampi of AD patients has also been recently shown 49 . Interestingly, in TLR2-deficient mice, IH resulted in more prominent upregulation of this molecule (SI Fig.…”

Lipopolysaccharide-stimulated, NF-kB-, miRNA-146a- and miRNA-155-mediated molecular-genetic communication between the human gastrointestinal tract microbiome and the brain

“…It is currently not well understood if GI-tract barrier-disrupting proteolytic endotoxins such as BFT are able to propagate pathogenic actions via the systemic circulation to further disrupt the blood-brain barrier and transfer LPS, BFT, and other endotoxins into the cerebrovascular circulation to the brain parenchyma, neural cells and synaptic circuitry of the CNS. However, it has recently been reported that BF-LPS, BFT and amyloid peptides progressively alter neural cytoarchitecture, synaptic adhesion, affecting both the function and integrity of synapses -a series of processes that play critical roles in the disruption of functional inter-neuronal signaling throughout neuronal networks in AD [33,39,42,48,57,65,76].…”

The Innate Immune Toll-Like Receptor-2 modulates the Depressogenic and Anorexiolytic Neuroinflammatory Response in Obstructive Sleep Apnoea

“…Finally, neuroplastin is known to play a role in synaptic plasticity (e.g. long-term potentiation), formation and a balance of the excitatory/inhibitory synapses (46), in shaping of brain's cortical thickness (47), and its involvement in early tissue response in hippocampi of AD patients has also been recently shown (48). Representative images of control (A-C) and animals exposed to IH (D-F) at 72 hours.…”