One reason I hate discussing vaccines with an anti vaxer is because they won't go do their homework. They'll find some small print somewhere in a study then misguide it to their agenda.

In the Michigan study (the first-ever to link “virus serology and brain autoantibody in autism”), the researchers measured exposure, via antibodies, to measles virus and human herpesvirus-6 in 48 autistic children and 34 controls, and simultaneously assessed levels of two key brain autoantibodies. What they found—unusually high levels of autoantibodies in the autistic children suggestive of an autoimmune response—particularly held true in association with measles virus, and “the higher the virus antibody titer the greater the chance of brain autoantibody.” Addressing the question of how exposure to measles virus occurred in the first place, the authors remarked, “virtually all subjects in the study had their MMR immunizations and none had any history of wild-type measles virus infection.”

What it really said:

We found that measles-IgG and HHV-6-IgG titers were moderately higher in autistic children but they did not significantly differ from normal controls.

Whole paragraph:

Considering an autoimmunity and autism connection, brain autoantibodies to myelin basic protein (anti-MBP) and neuron–axon filament protein (anti-NAFP) have been found in autistic children. In this current study, we examined associations between virus serology and autoantibody by simultaneous analysis of measles virus antibody (measles-IgG), human herpesvirus-6 antibody (HHV-6-IgG), anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG titers were moderately higher in autistic children but they did not significantly differ from normal controls. Moreover, we found that a vast majority of virus serology-positive autistic sera was also positive for brain autoantibody: (i) 90% of measles-IgG-positive autistic sera was also positive for anti-MBP; (ii) 73% of measles-IgG-positive autistic sera was also positive for anti-NAFP; (iii) 84% of HHV-6-IgG-positive autistic sera was also positive for anti-MBP; and (iv) 72% of HHV-6-IgG-positive autistic sera was also positive for anti-NAFP. This study is the first to report an association between virus serology and brain autoantibody in autism; it supports the hypothesis that a virus-induced autoimmune response may play a causal role in autism.

Did you bother to go look at what autoantibodies were?

They are monoclonal antibodies, meaning naturally occurring, there was no "measles" vaccines involved in this study but rather they looked at the pathology to try and answer why some monoclonal autoantibodies could be escaping the BBB and entering the brain. They mentioned there is a probability this happens during fetal brain development when the brain isn't fully developed yet. This escape, however in the end they could come to a conclusive determination....meaning in the future of their research, may end up conclusively determining neurological disorders with one of them being autism listed.

In summary:

Determining the mechanism of action and pathogenicity of several brain-reactive autoantibodies could facilitate more accurate and rapid diagnosis and enable novel treatment options. Here, we describe two examples of autoimmune diseases, which are mediated, at least in part, by autoantibodies and their pathology is well characterized. Both antibodies in those diseases are targeting extracellular antigens on brain cells, either neurons or astrocytes, but differ in their mechanism(s) of action, and hence their pathology.

Anti-DNA/anti-NMDA receptor antibodies in SLE are targeting neurons, resulting in neuronal cell death by enhancing NMDAR activation. Depending on the localization of BBB impairment, DNRAbs result in different neurocognitive or neurobehavioral phenotypes. There is no CNS inflammation following acute exposure to DNRAbs. The sustained, chronic state of neuronal damage secondary to neuronal death that persists after antibody exposure is no longer present in the CNS may reflect either neuron intrinsic effects secondary to antibody exposure or microglial activation.

Brain antibodies in NMO bind to the astrocyte water channel protein AQP4 and result in irreversible astrocyte damage due to CDCC or ADCC. There is increasing evidence that AQP4-IgG can also act by themselves and result in reversible internalization of the AQP4-IgG complex, which is coupled to the excitatory amino acid transporter (EAAT2) endocytosis (94). Different mechanisms might contribute to reversible and irreversible tissue damage of NMO patients [Figure 2, modified from Ref. (37)]. NMO is an example of an antibody-mediated disease where brain pathology of patients shows an inflammatory infiltrate in the CNS, yet, the role of pathogenic T cells in the disease pathogenesis remains to be investigated.

In order to enable appropriate and less invasive treatment, we need to understand the acute and chronic effects of antibody exposure.

https://www.frontiersin.org/articles/10.3389/fimmu.2017.01101/full

I could go over the other studies listed and waste another hour of my time but I am sure I'll find the same "hidden" items they don't post or look up words in the study I don't understand so I understand them and how they relate to what is going on.

May I suggest until the time that you decide to do the same don't come at me with anymore of your anti vaxer sites.