TEMPORALLY GRADED SEMANTIC MEMORY LOSS IN ALZHEIMER'S DISEASE: CROSS-SECTIONAL AND LONGITUDINAL STUDIES

2004 ◽  
Vol 21 (2-4) ◽  
pp. 353-378 ◽  
Author(s):  
Robyn Westmacott ◽  
Morris Freedman ◽  
Sandra E. Black ◽  
Kathryn A. Stokes ◽  
Morris Moscovitch
1991 ◽  
Vol 3 (2) ◽  
pp. 166-182 ◽  
Author(s):  
Kathryn A. Bayles ◽  
Cheryl K. Tomoeda ◽  
Alfred W. Kaszniak ◽  
Michael W. Trosset

Results of several prior studies, in which Alzheimer's disease (AD) patients missed the same concepts on multiple tasks, have been used to substantiate the theory that AD causes concept-specific loss of information from semantic memory However, sample sizes in these studies are modest, test-retest intervals small, and typically only a few tasks were used. In the present study 69 An subjects were annually administered 11 tasks, each using the same 13 concepts. Only a few instances were observed in which a concept was missed across all 11 tasks. When performances on the Oral Reading and Dictation tasks were removed from analysis, because of their questionable reliance on semantic memory, the number of missed concepts rose only modestly. A substantial rise in the number of missed concepts occurred, however, when performances on the four multiple- choice tasks were removed. Interpreting the larger number of missed concepts on the five remaining generative semantic tasks as evidence of item-specific loss is problematic, nonetheless, because the generative semantic tasks were among the hardest in the battery and the frequency with which an individual subject missed a concept across all tasks accorded with the subject's dementia severity level. Results also indicate that task difficulty, more than concept specificity, determine whether a concept is missed. Overall, results suggest that a concept will “disappear” when all of the tasks in which it is a stimulus become too difficult for the patient to perform. Study results call into question the appropriateness of using batteries of effortful, attention demanding tasks for ascertaining whether AD causes item-specific loss of conceptual knowledge.


2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Kok Pin Ng ◽  
Hui Chiew ◽  
Pedro Rosa-Neto ◽  
Nagaendran Kandiah ◽  
Zahinoor Ismail ◽  
...  

AbstractThe development of in vivo biomarkers of Alzheimer’s disease (AD) has advanced the diagnosis of AD from a clinical syndrome to a biological construct. The preclinical stage of AD continuum is defined by the identification of AD biomarkers crossing the pathological threshold in cognitively unimpaired individuals. While neuropsychiatric symptoms (NPS) are non-cognitive symptoms that are increasingly recognized as early manifestations of AD, the associations of NPS with AD pathophysiology in preclinical AD remain unclear. Here, we review the associations between NPS and AD biomarkers amyloid-β (Aβ), tau and neurodegeneration in preclinical AD and cognitively-unimpaired individuals in 19 eligible English-language publications (8 cross-sectional studies, 10 longitudinal, 1 both cross-sectional and longitudinal). The cross-sectional studies have consistently shown that NPS, particularly depressive and anxiety symptoms, are associated with higher Aβ. The longitudinal studies have suggested that greater NPS are associated with higher Aβ and cognitive decline in cognitively unimpaired subjects over time. However, most of the studies have either cross-sectionally or longitudinally shown no association between NPS and tau pathology. For the association of NPS and neurodegeneration, two studies have shown that the cerebrospinal fluid total-tau is linked to longitudinal increase in NPS and that the NPS may predict longitudinal metabolic decline in preclinical AD, respectively. However, evidence for the association between atrophy and NPS in preclinical AD is less consistent. Therefore, future longitudinal studies with well-designed methodologies and NPS measurements are required not only to determine the relationship among AT(N) biomarkers, NPS and cognitive decline, but also to elucidate the contribution of comorbid pathology to preclinical AD.


Author(s):  
T.J. Littlejohns ◽  
K. Kos ◽  
W.E. Henley ◽  
E. Kuma ◽  
D.J. Llewellyn

Emerging evidence suggests that low vitamin D concentrations are potentially involved in the pathogenesis of dementia. This is of particular interest when considering the high prevalence of vitamin D deficiency in elderly adults and the urgent need to identify modifiable risk factors for dementia. Studies have found that vitamin D is implicated in procognitive and neuroprotective functions, including the reduction of Alzheimer’s disease hallmarks such as amyloid beta and phosphorylated tau. Cross-sectional studies have consistently found that vitamin D concentrations are significantly lower in individuals with Alzheimer’s disease and cognitive impairment compared to healthy controls. Longitudinal studies support an association between low vitamin D concentrations and an increased risk of dementia and cognitive decline. Neuroimaging studies are beginning to uncover the potential neurodegenerative and cerebrovascular mechanisms that underlie these associations such as white matter hyperintensities and enlarged ventricular volume, although there is currently a lack of longitudinal studies. In contrast to observational studies, findings from interventional studies have produced mixed results on the benefits of vitamin D supplementation on dementia and cognitive outcomes. Interpretation of the findings from these studies is hampered by several major methodological limitations, such as small sample sizes, inadequate doses and inclusion of participants unlikely to benefit from vitamin D supplementation. There is a need for large double-blind randomised-control trials investigating whether vitamin D supplementation can halt or delay the risk of dementia-related outcomes in individuals with low vitamin D concentrations.


2010 ◽  
Vol 6 ◽  
pp. S524-S524
Author(s):  
Fei Song ◽  
Anne Poljak ◽  
Michael Valenzuela ◽  
George A. Smythe ◽  
Perminder S. Sachdev

Dementia ◽  
2018 ◽  
Vol 19 (3) ◽  
pp. 847-860 ◽  
Author(s):  
Cathy B Scott ◽  
Olivio J Clay ◽  
Fayron Epps ◽  
Fawn A Cothran ◽  
Ishan C Williams

Caring for an individual living with Alzheimer’s disease and other forms of dementia is especially challenging and impacts every aspect of the lives of the family caregivers. Family caregiving is defined as informal, unpaid care provided by family or friends to people with a chronic illness or disability. Caregiver burden, often experienced by a caregiver for a cognitively impaired family member, is multifaceted involving physical, psychological, social, and emotional problems. To date, little has been done to examine the relationship between the knowledge of Alzheimer’s disease and memory loss and caregiver burden. To fill this gap, a cross sectional, correlational design was employed to collect data from a convenience sample ( N = 104) of African American and Caucasian dementia family caregivers. For this study, caregivers ranged from 25 to 89 years of age with African American caregivers possessing significantly lower levels of knowledge about Alzheimer’s disease and other dementias compared to Caucasian caregivers, p < .001. There were 44 caregivers who scored 41 or greater on the Caregiver Burden Inventory corresponding to moderate to severe and higher levels of burden. Results of hierarchical multiple regression models indicated that higher levels Alzheimer’s disease knowledge was significantly associated with lower caregiver burden for all caregivers, B = −0.294, p < .01. Additionally, employment status was significantly associated with caregiver burden. This study highlights the benefits of including disease specific knowledge within educational components of dementia related interventions and programs involving families.


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