Cognitive Profiles of Autopsy-Confirmed Lewy Body Variant vs Pure Alzheimer Disease

Connor, Donald J.; Salmon, David P.; Sandy, Teresa J.; Galasko, Douglas; Hansen, Lawrence A.; Thal, Leon J.

doi:10.1001/archneur.55.7.994

Cited by 113 publications

(100 citation statements)

References 32 publications

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“…No 2-year decline in FTD Comparison AD-LBD Nervi [152] Figure copying LBD worse than AD Crowell [153] Figure copying LBD worse than AD Tiraboschi [154] Figure copying LBD worse than AD; no differences in pentagon copying Cahn-Wiener [156] CDT No differences in overall score, but more conceptual and planning errors in LBD Hamilton [157] Clock copying No differences, but lower scores predicted steeper decline in LBD Cagnin [158] CDT LBD worse than AD Palmqvist [159] CDT, cube copying LBD worse than AD Gnanalingham [162] CDT, clock copying No difference in CDT; LBD worse than AD in clock copying Ala [164] Pentagon copying LBD worse than AD Cormack [165] Pentagon copying LBD worse than AD Connor [166] Pentagon copying No difference Caffarra [167] Figure copying, No difference in figure copying, pentagon copying worse scores in LBD on an analytic scoring system for pentagon copying AD, Alzheimer's disease; VaD, vascular dementia; sVaD, subcortical VaD; FTD, frontotemporal dementia; bvFTD, behavioral variant of FTD; PA, progressive aphasia; LBD, Lewy body dementia; CDT, Clock drawing test; ROCF, copy of Rey's complex figure. Reference numbering follows the text.…”

Section: Drawing Disorders In Vascular Dementiamentioning

confidence: 99%

Drawing Disorders in Alzheimer’s Disease and Other Forms of Dementia

Trojano

Gainotti

2016

JAD

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Abstract. Drawing is a multicomponential process that can be impaired by many kinds of brain lesions. Drawing disorders are very common in Alzheimer's disease and other forms of dementia, and can provide clinical information for the distinction of the different dementing diseases. In our review we started from an overview of the neural and cognitive bases of drawing, and from a recollection of the drawing tasks more frequently used for assessing individuals with dementia. Then, we analyzed drawing disorders in dementia, paying special attention to those observed in Alzheimer's disease, from the prodromal stages of the amnesic mild cognitive impairment to the stages of full-blown dementia, both in the sporadic forms with late onset in the entorhino-hippocampal structures and in those with early onset in the posterior neocortical structures. We reviewed the drawing features that could differentiate Alzheimer's disease from vascular dementia and from the most frequent forms of degenerative dementia, namely frontotemporal dementia and Lewy body disease. Finally, we examined some peculiar aspects of drawing disorders in dementia, such as perseverations, rotations, and closing-in. We argue that a careful analysis of drawing errors helps to differentiate the different forms of dementia more than overall accuracy in drawing.

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Section: Drawing Disorders In Vascular Dementiamentioning

confidence: 99%

Drawing Disorders in Alzheimer’s Disease and Other Forms of Dementia

Trojano

Gainotti

2016

JAD

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“…5,6 In contrast to this stereotypical pattern, Lewy bodies in AD may also be found concentrated in the amygdala without significant involvement of the brainstem or neocortical regions, 2,3 a distribution that has been called AD with amygdala Lewy bodies. 3,7 These cases with both Lewy body and AD pathology are 8,1418 There is controversy as to whether there are differences in parkinsonian features, 8,14,16,19,20 cognitive deficits, 16,17,[19][20][21] cognitive decline, 8,14 and the presence of visual hallucinations 8,17,18,20,22 between AD with Lewy bodies and AD without Lewy bodies (eTable in the Supplement). These diverse findings may partly reflect the relatively small sample sizes used in some of these studies or the limitations with the clinical or neuropathological data.…”

Section: Main Outcomes and Measures-clinical And Neuropsychiatric Tesmentioning

confidence: 99%

P1‐206: Clinical features of Alzheimer disease with and without lewy bodies

Chung

Babulal

Monsell

et al. 2015

Alzheimer's & Dementia

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edu).Role of the Funder/Sponsor: The funders/sponsors had no role in the design and conduct of the study; collection, management, analysis, or interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.Supplemental content at jamaneurology.com Author Contributions: Dr Morris had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Conflict of Interest Disclosures:Dr Morris has participated or is currently participating in clinical trials of antidementia drugs sponsored by the following companies and studies: Janssen Immunotherapy, Pfizer, Eli Lilly/Avid Radiopharmaceuticals, the SNIFF (Study of Nasal Insulin to Fight Forgetfulness) study, and the A4 (Anti-Amyloid Treatment in Asymptomatic Alzheimer's Disease) trial. Dr Morris has served as a consultant for Lilly USA, ISIS Pharmaceuticals, and the Charles Dana Foundation. He receives research support from Eli Lilly/Avid Radiopharmaceuticals and is funded by National Institutes of Health grants P50AG005681, P01AG003991, P01AG026276, and U19AG032438.Additional Information: The NACC database is funded by NIA/National Institutes of Health grant U01 AG016976. The NACC data were obtained from the NIA-funded AD centers (grants P30 AG019610 [PI Eric Reiman, MD] EXPOSURES-Standardized neuropathologic assessment and then brain autopsy after death. HHS Public Access MAIN OUTCOMES AND MEASURES-Clinical and neuropsychiatric test scores.RESULTS-The mean (SD) age at death was statistically significantly younger for participants who had AD with Lewy bodies (77.9 [9.5] years) than for participants who had AD without Lewy bodies (80.2 [11.1] years) (P = .01). The mean (SD) age at onset of dementia symptoms was also younger for participants who had AD with Lewy bodies (70.0 [9.9] years) than for participants who had AD without Lewy bodies (72.2 [12.3] years) (P = .03). More men than women had AD with Lewy bodies (P = .01). The frequency of having at least 1 APOE ε4 allele was higher for participants who had AD with Lewy bodies than for participants who had AD without Lewy bodies (P = .03). CONCLUSIONS AND RELEVANCE-Participants with both AD and Lewy body pathology have a clinical phenotype that may be distinguished from AD alone. The frequency of Lewy bodies in AD and the association of Lewy bodies with the APOE ε4 allele suggest potential common mechanisms for AD and Lewy body pathologies.The 2 neuropathological hallmarks of Alzheimer disease (AD) are the extracellular Aβ plaques and the intracellular neurofibrillary tangles, of which the latter is composed of hyperphosphorylated tau protein. 1 Lewy bodies are intraneuronal cytoplasmic inclusions comprising aggregates of α-synuclein 2,3 and are readily detected by immunohistochemistry using anti-α-synuclein antibodies. In up to 50% of cases of sporadic late-onset AD, comorbid Lewy bodies are found. 2 Lewy bodies are frequent in the setting of moderate-tosevere levels of A...

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“…These features, together with parkinsonism and the above mentioned visual hallucinations, are the main characteristics of dementia with Lewy bodies (DLB), possibly accounting for 15-20% of the dementias (McKeith, 1996). Indeed, PDD and DLB share many clinical (Ballard, 2002;Connor, 1998;Dubois, 1997) and pathological (Harding, 2001) features and are often difficult to distinguish other than by the temporary onset of dementia and psychosis in relation to parkinsonism (Richard, 2002). Therefore, Parkinson's disease and dementia with Lewy bodies are often considered to be part of the same disease spectrum (Burn, 2003a;Ballard, 2000;McKeith, 2000b), although this matter is still under considerable debate (Litvan, 1998).…”

Section: Dementia In Pdmentioning

confidence: 99%

Cognitive dysfunction and dementia in Parkinson?s disease

2004

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Summary. Parkinson's disease (PD) is a slowly progressive neurodegenerative disorder mainly characterized by degeneration of dopaminergic neurons in the substantia nigra and the ventral tegmental area, in combination with a varying loss of central noradrenergic (locus coeruleus), cholinergic (nucleus basalis of Meynert) and serotonergic (dorsal raphe nuclei) integrity, leading to a multitude of motor and non-motor behavioral disturbances.Apart from the clinical motor hallmarks, in the early stages of disease, subtle cognitive dysfunction might be seen comprising mainly executive dysfunction, with secondary visuospatial and mnemonic disturbances. In about 20-40% of patients, these problems may eventually proceed to dementia, which constitutes an important risk factor for caregiver distress, decreased quality of life and nursing home placement. Dementia in PD is typically characterized by a progressive dysexecutive syndrome with attentional deficits and fluctuating cognition, often accompanied by psychotic symptoms. It is thought to be the result of a combination of both subcortical and cortical changes. PD-related dopaminergic deficiency in the nucleus caudatus and mesocortical areas (due to degeneration of projections from the substantia nigra and ventral tegmental area) and cholinergic deficiency in the cortex (due to degeneration of ascending projections from the nucleus basalis of Meynert), combined with additional Alzheimer-pathology and cortical Lewy bodies, may greatly contribute to dementia.Current treatment of dementia in PD is based on compensation of the profound cholinergic deficiency. Recent studies with the cholinesterase inhibitors galantamine, donepezil and rivastigmine show promising results in improving cognition and ameliorating psychotic symptoms, which must further be confirmed in randomized controlled trials.

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Cognitive Profiles of Autopsy-Confirmed Lewy Body Variant vs Pure Alzheimer Disease

Cited by 113 publications

References 32 publications

Drawing Disorders in Alzheimer’s Disease and Other Forms of Dementia

Drawing Disorders in Alzheimer’s Disease and Other Forms of Dementia

P1‐206: Clinical features of Alzheimer disease with and without lewy bodies

Cognitive dysfunction and dementia in Parkinson?s disease

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