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Writing in 2006, on
the occasion of the
100th anniversary of Alloys
Alzheimer’s first description
of Alzheimer’s Dementia (AD),
Dr K Jellinger of the Institute
of Clinical Neurobiology,
Vienna noted ‘that despite
considerable progress in the
clinical diagnosis, neuroimaging,
genetics, molecular biology,
neuropathology, defining risk
factors, and treatment, the
etiology of the disease is still
unknown and, therefore, a
causal treatment of AD will not
be available in the near future.’
Similar absences mark studies
of other notable cognitive
diseases, like schizophrenia,
suggesting that current models
and experimental studies may
be directed to non-etiological
features of the diseases.
Significantly, cognitive diseases
display both mental and physical
symptomatic signatures.
Hence, new conceptions on
what is being progressively
impaired in these diseases
are needed to underwrite
therapeutic advances both for
the restoration of mental as
well as physical health. Such
inferences are likely to come
from studies on the brain’s
global regulation since a key
symptom of these diseases
is a pathological progression
in the loss of self-perception.
Existing studies reveal, for
example, that a fundamental
brain network needed for the
self construct, the default mode
network (DMN), which is critical
to monitoring the external
environment, bodily states, and
even emotions, is impaired in
AD. Furthermore, functional
MRI shows that activity in the
posterior cingulate and right
inferior temporal cortex and
that in the bilateral inferior
parietal cortex, are differentially
affected, reflecting a weakening
of causally influential relations
amongst the DMN principal
nuclei. Schizophrenia patients,
on the other hand, display
an inability to identify selfinitiated
actions, which is
likely due to a failure to link
self-representations to the
body, that may originate
in the DMN and premotor
cortices. Therapeutic
strategies that enhance the
neural underpinning of selfrepresentation
may, therefore,
delay symptomatic progression
in these diseases. Increasing
evidence suggests that practices
that enhance self-integration,
like contemplation, may assist
in strengthening these features.
This talk will discuss current
research on the impact of
these cognitive diseases on
the neural representation of
the self, and the potential use
of the contemplative practice
in strengthening the selfrepresentation
and delaying the
symptomatic onset.
Biography
Denis Larrivee is a Visiting Scholar at the Mind and Brain Institute, University of Navarra Medical School and Loyola University Chicago and has held professorships at the Weill Cornell University Medical College, NYC, and Purdue University, Indiana. A former fellow at Yale University’s Medical School he received the Association for Research in Vision and Ophthalmology’s first place award for studies on photoreceptor degenerative and developmental mechanisms. He is the editor of a recently released text on Brain-Computer Interfacing with InTech Publishing and an editorial board member of the journals Annals of Neurology and Neurological Sciences (USA) and EC Neurology (UK). An International Neuroethics Society Expert he is the author of more than 70 papers and book chapters in such varied journals/venues as Neurology and Neurological Sciences (USA), EC Neurology (UK), Journal of Neuroscience, Journal of Religion and Mental Health, and IEEE Explore. In 2018 he was a finalist in the international Joseph Ratzinger Expanded Reason award.