To determine if Alzheimer's disease (AD), its Lewy body (LB) variant (LBV), and diffuse LB disease (DLBD) are distinguishable at initial clinical evaluation, data from autopsy-confirmed AD, LBV, and DLBD were examined. No significant differences were found in age at onset, age at death, total duration of illness, duration of illness before initial visit, duration of illness from initial visit to death, or severity of illness at initial evaluation. Hallucinations and delusions were significantly more frequent for LBV and DLBD, respectively, than for AD, and falls were more frequent for DLBD than for AD. Extrapyramidal symptoms (EPS) were less frequent in neuroleptic-free AD subjects than in LB subjects; the percentage of AD patients with EPS after neuroleptic exposure was less than that among LB patients. Seizures were significantly more common for DLBD than for AD or LBV. LB dementias differed from AD at initial evaluation, with more frequent hallucinations and delusions, EPSs, and seizures, and longitudinally in neuroleptic sensitivity, but the data did not distinguish LBV from DLBD.
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http://dx.doi.org/10.1177/0891988703258671 | DOI Listing |
Am J Pathol
December 2010
Graduate Program in Molecular Biophysics, Department of Physiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA.
The pathological hallmark of Parkinson's disease and diffuse Lewy body disease (DLBD) is the aggregation of α-synuclein (α-syn) in the form of Lewy bodies and Lewy neurites. Patients with both Alzheimer's disease (AD) and cortical Lewy pathology represent the Lewy body variant of AD (LBV) and constitute 25% of AD cases. C-terminally truncated forms of α-syn enhance the aggregation of α-syn in vitro.
View Article and Find Full Text PDFJ Geriatr Psychiatry Neurol
December 2003
Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas 75390-9070, USA.
To determine if Alzheimer's disease (AD), its Lewy body (LB) variant (LBV), and diffuse LB disease (DLBD) are distinguishable at initial clinical evaluation, data from autopsy-confirmed AD, LBV, and DLBD were examined. No significant differences were found in age at onset, age at death, total duration of illness, duration of illness before initial visit, duration of illness from initial visit to death, or severity of illness at initial evaluation. Hallucinations and delusions were significantly more frequent for LBV and DLBD, respectively, than for AD, and falls were more frequent for DLBD than for AD.
View Article and Find Full Text PDFNeurology
January 2000
Neurologia Prima, Ospediali Riuniti, Bergamo, Italy.
Objective: To evaluate cholinergic activity in diseases with Lewy bodies (LB; LB variant of AD [LBV], diffuse LB disease [DLBD], and Parkinson's disease [PD]) to determine if 1) AD changes are requisite to cholinergic dysfunction, 2) cholinergic activity declines to the same extent in neocortical and archicortical areas, and 3) cholinergic loss is influenced by APOE genotype.
Background: Like AD, diseases with LB are associated with decreased choline acetyltransferase (ChAT) activity. Increased APOE epsilon4 allele frequency has been reported in LBV.
J Neuropathol Exp Neurol
May 1997
Department of Neurosciences, University of California, San Diego, La Jolla 92093-0624, USA.
Dementia with Lewy bodies (DLB) is the second leading cause of cognitive impairment among the elderly. While it is usually accompanied by the neocortical neuritic plaques (NP) and entorhinal neurofibrillary tangles (NFT) characteristic of Alzheimer disease (AD), and so can be construed as a Lewy body variant of AD (LBV), it also occurs in pure form as diffuse Lewy body disease (DLBD). We assessed cognitive status in 17 DLB patients (12 with LBV and 5 with DLBD) and compared the results with 12 AD subjects and 5 controls.
View Article and Find Full Text PDFNeurosci Lett
February 1997
Department of Neurosciences, University of California, San Diego, USA.
The Lewy body variant of Alzheimer disease (LBV) is a distinct category of dementia which, unlike pure diffuse Lewy body disease (DLBD), meets clinical and neuropathologic criteria for Alzheimer disease (AD) but differs from pure AD in having a neocortical predominance of diffuse and neuritic plaques (NP), with very few neurofibrillary tangles (NFT). We investigated the immunoreactivity of NP with a monoclonal antibody against paired helical filaments (PHF) composed of phosphorylated microtubule associated protein tau. With routine thioflavin-S preparations, 12 LBV and 14 AD cases had similar numbers of NP, but the LBV had significantly (P < 0.
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