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To: tired&retired
Sorry.. lost formatting.. Here is the person who made the statement I repeated. He is one of the leading brain researchers in the world. I attended his lecture in August of this year at a psychiatric conference. I'll scan his work as I have his power-point slides and references.

http://www.upmc.com/media/experts/Pages/david-a-lewis.aspx

David A. Lewis, MD ​UPMC Endowed Professor in Translational Neuroscience and Chair, Psychiatry, University of Pittsburgh Schools of the Health Sciences ​David A. Lewis, MD was named chair of the University of Pittsburgh Department of Psychiatry and Medical Director of the Western Psychiatric Institute and Clinic of UPMC in September 2009. A national expert in schizophrenia, Dr. Lewis’ research focuses on the neural circuitry of the prefrontal cortex and related brain regions and the alterations of this circuitry in schizophrenia.

Dr. Lewis is the UPMC Professor of Translational Neuroscience in the Department of Psychiatry, School of Medicine; professor of neuroscience in the School of Arts and Sciences; and director of the Translational Neuroscience Program at the University of Pittsburgh. In addition to his academic responsibilities, Dr. Lewis serves as director of a National Institute of Mental Health (NIMH) Conte Center for the Neuroscience of Mental Disorders at Western Psychiatric Institute and Clinic, which is focused on understanding the role of prefrontal cortical dysfunction in the pathophysiology of schizophrenia.

Dr. Lewis received his Bachelor of Arts in psychology and his medical degree from The Ohio State University. After completing residencies in internal medicine and psychiatry at the University of Iowa, Dr. Lewis received his research training at the Research Institute of the Scripps Clinic in California. He arrived in Pittsburgh in 1987 as associate professor of psychiatry and behavioral neuroscience. He has been the UPMC professor of translational neuroscience since 2006. An author of more than 300 scientific articles, Dr. Lewis serves as deputy editor of The American Journal of Psychiatry and a section editor of Neurobiology of Disease.

In 2007, he was appointed to the Institute of Medicine of the National Academy of Sciences for his contributions to the advancement of schizophrenia treatments and his efforts to bring the importance of this major public health issue to the forefront. He also has received the Leiber Prize from NARSAD, the Dean Award from the American College of Psychiatry and the Warren Award from the International Congress on Schizophrenia Research, each of which recognizes major contributions to advancing the understanding of schizophrenia.

47 posted on 10/24/2017 4:37:27 AM PDT by tired&retired (Blessings)
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To: tired&retired

Dementia as a complication of schizophrenia
P J de Vries, W G Honer, P M Kemp, P J McKenna

J Neurol Neurosurg Psychiatry 2001;70:588–596

Abstract
Objectives—Cognitive impairment is
known to occur in schizophrenia, and may
be marked in institutionalised patients.
The aim of this study was to determine
whether it ever warrants an additional
diagnosis of dementia.

Conclusions—Dementia in schizophrenia
seems to be a real entity with a neuropsychological
signature similar to that of
frontotemporal dementia. Functional but
not structural imaging abnormalities may
also be characteristic.
(J Neurol Neurosurg Psychiatry 2001;70:588–596)

The coincidental development of Alzheimer’s
disease, multi-infarct dementia, or cortical
Lewy body disease in some of the older patients
is diffcult to exclude with certainty during life,
and CT appearances may be deceptively
normal in Alzheimer’s disease.52

However, there are reasons for doubting that the patients
had any of these disorders: (a) Alzheimer’s disease
is rare in the presenile period; (b) medial
temporal lobe atrophy was no greater in this
series of patients than in schizophrenia as a
whole; (c) multi-infarct dementia would be
unusual in the absence of other evidence of
vascular disease; and (d) all three dementias
would be likely to progress rather than remain
static over periods of observation ranging from
2 to 10 years. One further dementia, frontotemporal
dementia, remains a realistic differential
diagnosis: this commonly presents in the
presenile period, may progress only slowly, and
may show functional imaging abnormalities
coupled with structural imaging appearances
which remain normal for a long time.53–55 A
counter argument, however, is that, on current
evidence, psychotic symptoms are uncommon
in frontotemporal dementia.55


48 posted on 10/24/2017 5:15:28 AM PDT by tired&retired (Blessings)
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