scholarly journals Longitudinal patterns of semantic and episodic memory in frontotemporal lobar degeneration and Alzheimer’s disease

2009 ◽  
Vol 16 (2) ◽  
pp. 278-286 ◽  
Author(s):  
SHARON X. XIE ◽  
DAVID J. LIBON ◽  
XINGMEI WANG ◽  
LAUREN MASSIMO ◽  
PEACHIE MOORE ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Free Recall ◽  
Semantic Memory ◽  
Frontotemporal Lobar Degeneration ◽  
Initial Assessment ◽  
Group Differences ◽  
Longitudinal Analyses ◽  
Longitudinal Patterns ◽  
Delayed Recognition

AbstractThe longitudinal assessment of episodic and semantic memory was obtained from 236 patients diagnosed with Alzheimer’s disease (AD, n = 128) and with frontotemporal lobar degeneration (FTLD, n = 108), including patients with a social comportment/dysexecutive (SOC/EXEC) disorder, progressive nonfluent aphasia (PNFA), semantic dementia (SemD), and corticobasal syndrome (CBS). At the initial assessment, AD patients obtained a lower score on the delayed free recall test than other patients. Longitudinal analyses for delayed free recall found converging performance, with all patients reaching the same level of impairment as AD patients. On the initial evaluation for delayed recognition, AD patients also obtained lower scores than other groups. Longitudinal analyses for delayed recognition test performance found that AD patients consistently produced lower scores than other groups and no convergence between AD and other dementia groups was seen. For semantic memory, there were no initial between-group differences. However, longitudinal analyses for semantic memory revealed group differences over illness duration, with worse performance for SemD versus AD, PNFA, SOC/EXEC, and CBS patients. These data suggest the presence of specific longitudinal patterns of impairment for episodic and semantic memory in AD and FTLD patients suggesting that all forms of dementia do not necessarily converge into a single phenotype. (JINS, 2010, 16, 278–286.)

Memory impairment in Alzheimer's disease: replication and extension of the delayed word recall (DWR) test

1996 ◽  
Vol 13 (2) ◽  
pp. 55-58 ◽  
Author(s):  
Robert F Coen ◽  
Gregory RJ Swanwick ◽  
Conor Maguire ◽  
Michael Kirby ◽  
Brian A Lawlor ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Free Recall ◽  
Recognition Performance ◽  
Word Recall ◽  
Control Subjects ◽  
Clinical Interest ◽  
Delayed Recognition ◽  
Sensitivity Specificity

AbstractObjective: The original DWR test, which measured delayed free recall, was reported to have high predictiveaccuracy in discriminating Alzheimer's disease (AD) patients from control subjects (overall accuracy of 95%).Comparison of differential performance in free recall and recognition of the same material may be of clinical interest. In the present study a delayed recognition component was added to the DWR test and the utility of both measures in discriminating AD patients from control subjects was evaluated.Procedure: This extended version of the DWR test was administered to 66 patients meeting NINCDS/ADRDA criteria for probable AD and 42 control subjects.Results: In a comparison between 42 of these patients (MMSE range 18–29), and 42 age matched healthy controls, both the delayed free recall and recognition measures were highly accurate in distinguishing patients from controls. The free recall measure achieved 98% sensitivity, specificity and overall accuracy, while the recognition measure yielded 98% sensitivity, 95% specificity, and 96% overall accuracy. The recognition performance of all 66 patients, ranging in severity from very mild to severe (MMSE range 11–29), was also evaluated to determine its relationship, if any, to measures of global cognitive impairment. While therecognition measure correlated poorly with MMSE and CAMCOG there was a modest but significant correlation with the CAMCOG memory subscale.Conclusions: In this study of highly selected AD patients both the free recall and recognition measures were sensitive and specific indicators of AD compared to control subjects. Recognition performance appears to be more closely related to degree of amnesia than to degree of global cognitive impairment.

CCL8/MCP-2 association analysis in patients with Alzheimer’s disease and frontotemporal lobar degeneration

2009 ◽  
Vol 256 (8) ◽  
pp. 1379-1381 ◽  
Author(s):  
Chiara Villa ◽  
Eliana Venturelli ◽  
Chiara Fenoglio ◽  
Francesca Clerici ◽  
Alessandra Marcone ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Analysis ◽  
Frontotemporal Lobar Degeneration

The Semantic Memory Impairment of Alzheimer's Disease: Category-Specific?

Cortex ◽  
1996 ◽  
Vol 32 (1) ◽  
pp. 143-153 ◽  
Author(s):  
Lynette J. Tippett ◽  
Murray Grossman ◽  
Martha J. Farah
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Semantic Memory ◽  
Memory Impairment ◽  
Disease Category

P4-093: Semantic memory impairment in Alzheimer's disease and frontotemporal dementia is associated with semantic network degradation

2011 ◽  
Vol 7 ◽  
pp. S734-S734
Author(s):  
Kimiko Domoto-Reilly ◽  
Daisy Sapolsky ◽  
Michael Brickhouse ◽  
Mark Hollenbeck ◽  
Brad Dickerson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Dementia ◽  
Semantic Memory ◽  
Memory Impairment ◽  
Semantic Network

scholarly journals The Role of the Innate Immune System in Alzheimer’s Disease and Frontotemporal Lobar Degeneration: An Eye on Microglia

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Elisa Ridolfi ◽  
Cinzia Barone ◽  
Elio Scarpini ◽  
Daniela Galimberti
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontotemporal Lobar Degeneration ◽  
Environmental Changes ◽  
Current Evidence ◽  
Neuronal Function ◽  
Immune Effector ◽  
Effector Cells ◽  
The Central Nervous System

In the last few years, genetic and biomolecular mechanisms at the basis of Alzheimer’s disease (AD) and frontotemporal lobar degeneration (FTLD) have been unraveled. A key role is played by microglia, which represent the immune effector cells in the central nervous system (CNS). They are extremely sensitive to the environmental changes in the brain and are activated in response to several pathologic events within the CNS, including altered neuronal function, infection, injury, and inflammation. While short-term microglial activity has generally a neuroprotective role, chronic activation has been implicated in the pathogenesis of neurodegenerative disorders, including AD and FTLD. In this framework, the purpose of this review is to give an overview of clinical features, genetics, and novel discoveries on biomolecular pathogenic mechanisms at the basis of these two neurodegenerative diseases and to outline current evidence regarding the role played by activated microglia in their pathogenesis.

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