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Page 19
ISSN:2171-6625
September 18-19, 2017 | Dallas, USA
4th International Conference on
NEUROLOGY AND NEUROIMMUNOLOGY
Adaptive lymphocyte profiles correlate to brain Aβ burden in patients with mild cognitive impairment
Ann M Stowe
UT Southwestern Medical Center, USA
Background: Wepreviously found that subjectswithamnestic
mild cognitive impairment exhibit a pro-inflammatory
immune profile in the cerebrospinal fluid similar to multiple
sclerosis, a central nervous system autoimmune disease. We
therefore hypothesized that early neuroinflammation would
reflect increases in brain amyloid burden during amnestic
mild cognitive impairment.
Methods: Cerebrospinal fluid and blood samples were
collected from 24 participants with amnestic mild
cognitive impairment (12 men, 12 women; 66±6y; 0.5
Clinical Dementia Rating) enrolled in the AETMCI study.
Analyses of cerebrospinal fluid and blood included immune
profiling by multi-parameter flow cytometry, genotyping
for apolipoprotein (APO)ε, and quantification of cytokine
and immunoglobin levels. Amyloid (A)β42 deposition
was determined by 18F-florbetapir positron emission
tomography. Spearman rank order correlations were
performed to assess simple linear correlation for parameters
including amyloid imaging, central and peripheral immune
cell populations, and protein cytokine levels.
Results: There was a significant decline in solube Aβ42 in
the cerebrospinal fluid as mean brain Aβ42 deposition,
as well as amyloid burden in the precuneus and posterior
cingulate cortices, increased. Lymphocyte profiling revealed
a significant decline in T cell populations in the cerebrospinal
fluid, specifically CD4+ T cells, as Aβ42 deposition in the
posterior cingulate cortex increased. In contrast, increased
Aβ42 burden correlated positively with increased memory
B cells in the cerebrospinal fluid, which was exacerbated in
APOε4 carriers. For peripheral circulating lymphocytes, only
B cell populations decreased with Aβ42 deposition in the
precuneus cortex, as peripheral T cell populations did not
correlate with changes in brain amyloid burden.
Conclusions: Elevations in brain Aβ42 burden associate with
a shift from T cells to memory B cells in the cerebrospinal
fluid of subjects with amnestic mild cognitive impairment in
this exploratory cohort. These data suggest the presence of
cellular adaptive immune responses during Aβ accumulation,
but further study needs to determine whether lymphocyte
populations contribute to, or result from, Aβ dysregulation
during memory decline on a larger cohort collected at
multiple centers.
Speaker Biography
Ann M Stowe has completed her PhD in Molecular & Intergrative Physiology from
the University of Kansas, and a Post-dotoral Fellowship fromWashington University
in St. Louis. She is currently an Assistant Professor in the Dept. of Neurology at
UT Southwestern Medical Center in Dallas. Her research focuses on the role of
neuroinflammation in CNS injury and repair in both preclinical mouse models of
stroke, as well as clinical studies involving patients with either stroke or amnestic mild
cognitive impairment (aMCI).
e:
Ann M Stowe, J Neurol Neurosci, 8:5
DOI: 10.21767/2171-6625-C1-002