Memory Impairment and Awareness of Memory Deficits inEarly-Stage Alzheimer's Disease

Stewart G, McGeown WJ, Shanks MF, Venneri A. Anosognosia for memory impairment in Alzheimer's disease.ObjectiveTo investigate whether patients with Alzheimer's disease (AD) were able to alter their awareness of memory deficits after exposure to a memory task.Methods:Thirty normal older adults and 23 mild AD patients participated in the study. Anosognosia was assessed using discrepancies between self- and informant-evaluations of cognitive and functional performance. Participants estimated their performance on the Verbal Paired Associates task at different points in time (before, immediately after the task and after a 1-h delay).Results:AD patients were generally less able to judge their memory abilities than healthy older adults, and tended to overestimate their task performance beforehand. Their prediction accuracy increased immediately after the task, but after a 1-h delay, they again misjudged their abilities at pretesting accuracy levels. Self-carer discrepancy scores of awareness of deficits in memory and other areas correlated significantly with memory tests but not with other neuropsychological tasks in the assessment, and larger discrepancy scores were associated with poorer performance.Conclusion:AD patients can monitor their task performance online, but are unable to maintain awareness of their deficits over time. Loss of awareness of memory deficits (or of any other deficits) in early stage AD may indicate damage to a system which updates a personal knowledge base with recent information. Failure to retain this information impedes abstraction from episodic to semantic memory.

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Memory Impairment and Awareness of Memory Deficits in Early-Stage Alzheimer's Disease

The Tohoku Journal of Experimental Medicine ◽

10.1620/tjem.215.133 ◽

2008 ◽

Vol 215 (2) ◽

pp. 133-140 ◽

Cited By ~ 13

Author(s):

Masaru Mimura

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Memory Impairment ◽

Early Stage ◽

Memory Deficits

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Non-Alzheimer's disease-related memory impairment and dementia

Dialogues in Clinical Neuroscience ◽

10.31887/dcns.2013.15.4/sarlt ◽

2013 ◽

Vol 15 (4) ◽

pp. 465-473 ◽

Cited By ~ 4

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Memory Impairment ◽

Clinical Symptoms ◽

Memory Function ◽

The Elderly ◽

Memory Deficits ◽

Common Cause ◽

Underlying Causes ◽

Therapeutic Possibilities

Although Alzheimer's disease (AD) is a common cause of memory impairment and dementia in the elderly disturbed memory function is a widespread subjective and/or objective symptom in a variety of medical conditions. The early detection and correct distinction of AD from non-AD memory impairment is critically important to detect possibly treatable and reversible underlying causes. In the context of clinical research, it is crucial to correctly distinguish between AD or non-AD memory impairment in order to build homogenous study populations for the assessment of new therapeutic possibilities. The distinction of AD from non-AD memory impairment may be difficult, especially in mildly affected patients, due to an overlap of clinical symptoms and biomarker alterations between AD and certain non-AD conditions. This review aims to describe recent aspects of the differential diagnosis of AD and non-AD related memory impairment and how these may be considered in the presence of memory deficits.

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Early Hippocampal Sharp-Wave Ripple Deficits Predict Later Learning and Memory Impairments in an Alzheimer’s Disease Mouse Model

10.1101/596569 ◽

2019 ◽

Author(s):

Emily A. Jones ◽

Anna K. Gillespie ◽

Seo Yeon Yoon ◽

Loren M. Frank ◽

Yadong Huang

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Spatial Memory ◽

Genetic Risk ◽

Memory Impairment ◽

Memory Loss ◽

Memory Deficits ◽

Power Reduction ◽

Memory Impairments ◽

Sharp Wave

SUMMARYAlzheimer’s disease (AD) is characterized by progressive memory loss, and there is a pressing need to identify early pathophysiological alterations that predict subsequent memory impairment. Hippocampal sharp-wave ripples (SWRs) – electrophysiological signatures of memory reactivation in the hippocampus – are a compelling candidate for doing so. Mouse models of AD show reductions in both SWR abundance and associated slow gamma (SG) power during aging, but these alterations have yet to be directly linked to memory impairments. In aged apolipoprotein E4 knock in (apoE4-KI) mice – a model of the major genetic risk factor for AD – we found that reduced SWR abundance and associated CA3 SG power predicted spatial memory impairments measured 1–2 months later. Importantly, SWR-associated CA3 SG power reduction in young apoE4-KI mice also predicted spatial memory deficits measured 10 months later. These results establish features of SWRs as potential functional biomarkers of memory impairment in AD.

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Dimethyl fumarate attenuates working memory deficits in both young and old rats in the streptozotocin-induced model of sporadic Alzheimer’s disease

10.26226/morressier.5785edcfd462b80296c99f5f ◽

2016 ◽

Author(s):

Ewelina Kurowska

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Working Memory ◽

Dimethyl Fumarate ◽

Memory Deficits ◽

Sporadic Alzheimer’S Disease ◽

Old Rats

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Faculty Opinions recommendation of Inhibitors of class 1 histone deacetylases reverse contextual memory deficits in a mouse model of Alzheimer's disease.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.4693956.4576054 ◽

2010 ◽

Author(s):

Francine Benes ◽

Barbara Gisabella

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mouse Model ◽

Histone Deacetylases ◽

Memory Deficits ◽

Contextual Memory ◽

Model Of Alzheimer’S Disease ◽

Class 1

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Loss of ferroportin induces memory impairment by promoting ferroptosis in Alzheimer’s disease

Cell Death and Differentiation ◽

10.1038/s41418-020-00685-9 ◽

2021 ◽

Author(s):

Wen-Dai Bao ◽

Pei Pang ◽

Xiao-Ting Zhou ◽

Fan Hu ◽

Wan Xiong ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Memory Impairment ◽

Iron Homeostasis ◽

Critical Role ◽

Gene Set Enrichment Analysis ◽

Molecular Characteristics ◽

Intracellular Iron

AbstractIron homeostasis disturbance has been implicated in Alzheimer’s disease (AD), and excess iron exacerbates oxidative damage and cognitive defects. Ferroptosis is a nonapoptotic form of cell death dependent upon intracellular iron. However, the involvement of ferroptosis in the pathogenesis of AD remains elusive. Here, we report that ferroportin1 (Fpn), the only identified mammalian nonheme iron exporter, was downregulated in the brains of APPswe/PS1dE9 mice as an Alzheimer’s mouse model and Alzheimer’s patients. Genetic deletion of Fpn in principal neurons of the neocortex and hippocampus by breeding Fpnfl/fl mice with NEX-Cre mice led to AD-like hippocampal atrophy and memory deficits. Interestingly, the canonical morphological and molecular characteristics of ferroptosis were observed in both Fpnfl/fl/NEXcre and AD mice. Gene set enrichment analysis (GSEA) of ferroptosis-related RNA-seq data showed that the differentially expressed genes were highly enriched in gene sets associated with AD. Furthermore, administration of specific inhibitors of ferroptosis effectively reduced the neuronal death and memory impairments induced by Aβ aggregation in vitro and in vivo. In addition, restoring Fpn ameliorated ferroptosis and memory impairment in APPswe/PS1dE9 mice. Our study demonstrates the critical role of Fpn and ferroptosis in the progression of AD, thus provides promising therapeutic approaches for this disease.

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