Xins in both forms of dementia include TNF-a, arachidonic acid, platelet activating factors (PAF), nitric oxide (NO), and quinolinic acid (QUIN) [17,53-59]. Nitric oxide is synthesized by endothelial cells, neurons, and macrophages and is thought to be associated with NMDA-type glutamate-initiated neurotoxicity [54]. TNF-a is released by HIV-1-infected microglia, and oligodendrocytes are particula
The microglia signal transduction pathways mediating the neurotoxic response of Ab demonstrated that mitogen-activated protein-kinase (MAPK) superfamily members ERK1/2 and p38 MAPK act as mediators [95-97]. Furthermore, several lines of evidence indicate the NF-B in microglia is stimulated by b-amyloid [98,99]. Activation of NF-B can stimulate transcription of genes expressing TNF-a, IL-1, IL-6, m
Amyloid plaque deposition [39,42-44]. Indeed, most forms of dementia are accompanied by a widespread degeneration in the cerebral cortex - such as the plaques in AD brain. AD is thus considered a "cortical dementia." HAD is also considered to be a cortical dementia however there is also targeted damage to regions lying under the cortex. Some authors consider HAD to be a subcortical dementia howeve