E extent of immune activation in both blood and the brain and correlates with systemic and neurological disease status [17,53,55-59]. During immune activation, particularly while levels of IFN-g are increased, induction of the enzyme indoleamine 2,3-dioxygenase occurs, increasing the synthesis of QUIN [53,62-64]. HIV-infected microglia also release chemokines [65], which may enhance infiltration a
E extent of immune activation in both blood and the brain and correlates with systemic and neurological disease status [17,53,55-59]. During immune activation, particularly while levels of IFN-g are increased, induction of the enzyme indoleamine 2,3-dioxygenase occurs, increasing the synthesis of QUIN [53,62-64]. HIV-infected microglia also release chemokines [65], which may enhance infiltration a
Ycoprotein that is predominantly expressed by activated T cells, B cells, myeloid cells, and platelets. It has been well established that CD40L upregulates the immune response by leading to increased CD4+ T cell activation; an effect which promotes the replication of HIV in infected lymphocytes and immune cells [104] and also that robust CD40 ligation promotes an inflammatory and neurotoxic enviro
Ycoprotein that is predominantly expressed by activated T cells, B cells, myeloid cells, and platelets. It has been well established that CD40L upregulates the immune response by leading to increased CD4+ T cell activation; an effect which promotes the replication of HIV in infected lymphocytes and immune cells [104] and also that robust CD40 ligation promotes an inflammatory and neurotoxic enviro
E extent of immune activation in both blood and the brain and correlates with systemic and neurological disease status [17,53,55-59]. During immune activation, particularly while levels of IFN-g are increased, induction of the enzyme indoleamine 2,3-dioxygenase occurs, increasing the synthesis of QUIN [53,62-64]. HIV-infected microglia also release chemokines [65], which may enhance infiltration a
In both dementias. The initial step in each disease differs. HAD is secondary to infection with HIV-1, while the exact cause of AD remains to be established. A common feature among both diseases is the interactions of microglia which promote a neurotoxic inflammatory environment. These interactions play significant roles in the initiation and continuation of the neurodegenerative process in each d
In both dementias. The initial step in each disease differs. HAD is secondary to infection with HIV-1, while the exact cause of AD remains to be established. A common feature among both diseases is the interactions of microglia which promote a neurotoxic inflammatory environment. These interactions play significant roles in the initiation and continuation of the neurodegenerative process in each d
Y and also visibly damaged subcortical areas [45,46]. Amyloid plaques in AD result from the deposition of amyloid beta (Ab) which is a putative pathogenic molecule in AD. Ab is the cleavage product of the amyloid precursor protein (APP) and APP mutations are associated with inherited forms of AD. The clinical implication or pathogenic consequences of brain amyloid deposition are still controversia