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From: TSS ()
Subject: A sporadic case of Creutzfeldt Jakob disease with beta-amyloid deposits and alpha-synuclein inclusions
Date: July 26, 2007 at 9:27 am PST

Abstract

Case Report

A sporadic case of Creutzfeldt–Jakob disease with beta-amyloid deposits and
alpha-synuclein inclusions

Anne Vital,11Neuropathology Department, Victor Segalen – Bordeaux 2
University, Bordeaux,Anne Vital, MD, PhD, Laboratoire de Neuropathologie BP
42, Université Victor Segalen, Bordeaux 2, 146, rue Léo-Saignat, 33076
Bordeaux Cedex, France. Email: anne.vital@chu-bordeaux.fr Marie-Hélène
Canron,11Neuropathology Department, Victor Segalen – Bordeaux 2 University,
Bordeaux, Roger Gil,22Neurology Department, Poitiers University, Poitiers
and Jean-Jacques Hauw33Neuropathology Department, Pitié-Salpêtrière
Hospital, Paris, France and Claude Vital11Neuropathology Department, Victor
Segalen – Bordeaux 2 University, Bordeaux, 1Neuropathology Department,
Victor Segalen – Bordeaux 2 University, Bordeaux, 2Neurology Department,
Poitiers University, Poitiers and 3Neuropathology Department,
Pitié-Salpêtrière Hospital, Paris, France
Anne Vital, MD, PhD, Laboratoire de Neuropathologie BP 42, Université Victor
Segalen, Bordeaux 2, 146, rue Léo-Saignat, 33076 Bordeaux Cedex, France.
Email: anne.vital@chu-bordeaux.fr

Abstract

Neurodegenerative disorders are characterized by the correlation of clinical
symptoms and neuropathological changes in the brain. However, overlaps
between distinct entities are becoming more and more evident. We report the
coexistence of Alzheimer pathology and alpha-synuclein inclusions in a
sporadic, methionine/valine type 1, Creutzfeldt–Jakob disease (CJD) case.
There were neurofibrillary changes in the neocortex and beta amyloid
cerebral angiopathy was marked. Several Lewy bodies were present in the
substantia nigra, locus ceruleus and the dorsal motor nucleus of the vagus,
and alpha-synuclein cytoplasmic inclusions were also found in cortical
neurons. These findings raise the debated relationship between Parkinson’s
disease with dementia, dementia with Lewy bodies and a Lewy body variant of
Alzheimer disease. Among the factors that may have contributed to this
considerable morphological overlap are the patient’s age (79 years at
autopsy) and the over 2-year duration of the disease. As the average disease
duration in sporadic methionine/valine type 1 CJD is less than 6 months, it
seems legitimate to speculate that the initial symptoms resulted from
Alzheimer and alpha-synuclein related pathologies. This observation shows
that CJD can be present in elderly patients who are suspected of having
other neurodegenerative diseases, which could underline the importance of
neuropathology-based surveillance systems.


http://www.blackwell-synergy.com/doi/abs/10.1111/j.1440-1789.2007.00755.x

http://neurotalk.psychcentral.com/showthread.php?t=13175&page=2


Alzheimer's and Transmissible Spongiform Encephalopathies

http://neurotalk.psychcentral.com/showthread.php?t=13175


TSS





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