dementia-2019-keynote

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September 16-17, 2019 | Paris, France
Dementia and Alzheimer's Disease
13th World Congress on
Page 9
Journal of Clinical Psychiatry and Cognitive Psychology | Volume: 03
Alzheimer’s disease (AD) is an age-related multifactorial
progressive neurodegenerative disorder manifested
by memory loss, spatial disorientation, and gradual
deterioration of intellectual capacity. Its etiology is
unknown. Pathological changes including synaptic and
neuronal loss, oxidative damage, activated inflammatory
cells and protein depositions such as extracellular amyloid
plaques composed by misfolded amyloid beta (Aβ) peptide
and intracellular neurofibrillary tangles comprised of
hyperphosphorylated aggregates of the microtubule-
associated protein Tau ( ) are observed.
Compromised blood brain barrier (often observed at
AD) may permit increased contact of immune cells with
components released from dying neuronal cells, as well as
the transfer of various brain proteins into the blood and
induction of autoimmune response against them. Immune
system activation is frequently reported in patients
with AD. Some autoantibodies are naturally occurring
antibodies produced without extrinsic stimuli, originated
from B1 cells and reacting with various components
of neural system; however, antibodies derived after
antigenic stimulation by "self" might be produced by
B2 cells as well. Antibodies against Aβ, , neurofilament
light and heavy chains, S100B, cholinergic, adrenergic
and glutamatergic receptors, as well as some other brain-
derived antigens were reported in patients with various
should be stresssed that some level
of autoantibodies are comonly found at healthy individuals
and incomplete and often controversial results are reported
about CNS immune/autoimmune responses during AD.
Although autoantibodies might be sometime causing or
aggravating pathology, naturally occurring autoantibodies
may maintain physiological homeostasis, play key roles
in the clearance of self molecules and apoptotic cells,
protect from pathologically altered structures like
oxidatively damaged, aggregated, and non-functional
lipids and proteins. It is concievable as well, that impaired/
exhausted immune system of AD patients may contribute
to pathology. It is worth mentioning that autoantibodies
(or their specific profile) may serve as valuable biomarkers
of various neurodegenerative diseases.
In our report we will focuss on autoantibodies against in
AD, MCI and some other dementias, their charasterization
in heatlhy subjects, AD, MCI patients and some other
neurodegenerations, male/female differences and
potential application of intravenous imunoglobulin (IVIG)
treatent of neurodegenerative diseases.
Speaker Biography
Jan Ricny graduated from Faculty of Sciences, University of J.E. Purkyne,
Brno, Czechoslovakia in 1975 and obtained PhD from Institute of
Physiology, Czechoslovak Academy of Sciences, Prague in 1983. After
postdoctoral training at McGill university at Montreal and Max-Planck
Institut fur Biophysikalische Chemie at Gottingen works as researcher and
senior researcher at Institute of Physiology of Academy of Sciences and
National Institute of Mental Health, Czech Republic. Author of about 80
publications, H index 16. His main interests are cholinergic neurochemistry
and neurodegenerative diseases.
e:
Jan Ricny,
Kocurova G, Krestova M
National Institute of Mental Health, Czech Republic
Autoantibodies in Alzheimer´s disease