Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease

Alterations of hippocampal secreted N-CAM in bipolar disorder and synaptophysin in schizophrenia

“…26 This ratio has been Table 2 Summary of published and unpublished results for four N-CAM isoforms (VASE N-CAM, cytosolic N-CAM 105-115 kDa, SEC N-CAM, and membrane N-CAM 120-180 kDa) in the hippocampus of patients with schizophrenia or bipolar disorder as compared to controls 27 suggested to be a marker of synaptic maturity 26 and synaptic remodeling. 19,49 The origin of the cytosolic N-CAM 105-115 kDa is unknown 27 leaving the significance of the increased cytosolic N-CAM/synaptophysin ratio observed in patients with schizophrenia open to speculation. Synaptic plasticity is dependent upon functional and structural changes partially modulated by different N-CAM isoform expression.…”

Effects of transforming growth factor-beta on murine astrocyte glutamine synthetase activity. Implications in neuronal injury.

“…Although the mechanism of TGF-,3 enhancement of NMDA receptor-mediated neurotoxicity is unknown and is potentially complex, TGF-,B inhibition of astrocyte GS with an attendant reduction in metabolism of glutamate could be involved. Effects of Transforming Growth Factor-#f on Murine Astrocyte Glutamine Synthetase 1791 Cytokines produced during infection play an important role in inflammation and host defense (1)(2)(3)(4)(5)(6)(7)(8)(9). In the peripheral immune system, the immunologic functions of the proinflammatory cytokines (e.g., TNF-a, IL-1, and IL-6) are in many cases antagonized by the antiinflammatory cytokine TGF-,3 (29)(30)(31).…”

“…Recent studies suggest that cytokines play a pathogenetic role in a variety of central nervous system (CNS) diseases, including certain neurodegenerative disorders (1)(2)(3), autoimmune diseases (4,5), bacterial meningitis (6,7), and AIDS dementia (8,9). However, the mechanism by which cytokines mediate neuronal cell dysfunction, injury, and death is unknown.…”

Alzheimer disease and neuroplasticity: New approaches and new targets in pharmacotherapy

“…Especially for non-ApoE4 carriers and specific ethnic groups, this effect is well documented (100,101). A very interesting link is the fact that during aging and in AD, tau pathology starts in the entorhinal cortex and proceeds along the retrograde transport pathways of BDNF to the subiculum and CA1 subfield and then to the basal forebrain, amygdale and finally to several cortical regions (90). BDNF regulation is maintained through cholinergic innervations and through NMDA receptors (102,103).…”

“…Deregulations of proteins involved in structural plasticity of axons and dendrites indicate a failure of plasticity mechanisms, and support a disruption of synapse turnover as a primary mechanism in AD (15,89). Synaptic remodeling in AD is detected also by elevation in the NCAM/SNAP-25 (neural cell adhesion molecule /synaptosomal-associated protein of 25 kDa) ratio (76,90).…”