0000000000709730
AUTHOR
Susanne Otten
Mice with experimental antiphospholipid syndrome display hippocampal dysfunction and a reduction of dendritic complexity in hippocampal CA1 neurones
Aims The antiphospholipid syndrome (APS) is an autoimmune disease characterized by high titres of auto-antibodies (aPL) leading to thrombosis and consequent infarcts. However, many affected patients develop neurological symptoms in the absence of stroke. Similarly, in a mouse model of this disease (eAPS), animals consistently develop behavioural abnormalities despite lack of ischemic brain injury. Therefore, the present study was designed to identify structural alterations of hippocampal neurones underlying the neurological symptoms in eAPS. Methods Adult female Balb/C mice were subjected to either induction of eAPS by immunization with β2-Glycoprotein 1 or to a control group. After sixteen…
The experimental antiphospholipid syndrome: an invaluable tool to study autoimmunity-induced neurodegeneration
cells and its activation inhibits their differentiation and remyelination. These suggest a possible role of CNS TLR2 in progressive autoimmune demyelination. Methods: We examined the effects of intra-cerebro-ventricular (ICV) injection of Zymozan, a TLR2 agonist, on the clinical and pathological course of EAE. The survival and clinical scores were monitored; demyelination and axonal loss were quantified by gold-black and Bielschowsky stains, and the nature of neuro-inflammatory response was characterized by TLR2, IBA-1 and CD3 stainings and PCR for immune cytokines. Immune cells were isolated from EAE brain tissue and their proliferative response to the autoantigen (PLP peptide) or Concaval…