Anosognosia in Alzheimer's disease: diagnosis, frequency, mechanism and clinical correlates.

Cortex

Department of Psychiatry and Clinical Neurosciences, University of Western Australia and Fremantle Hospital, Western Australia, Australia. Electronic address:

Published: December 2014

Anosognosia is present in a large proportion of patients with mild Alzheimer's disease (AD), and its frequency increases with the progression of the illness. Several instruments have been validated to assess anosognosia in AD, but there is no consensus regarding the best diagnostic strategy. Anosognosia in AD is a significant predictor of apathy and is significantly related to lower depression and anxiety scores, more severe caregiver burden and dangerous behaviours. Studies using different imaging modalities have demonstrated an association between anosognosia and dysfunction in frontal, temporomedial and temporoparietal regions. The mechanism of anosognosia remains unknown, but it has been explained as a consequence of deficits of encoding and updating biographical memory, and dysfunction of comparator, executive and metacognitive systems.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.cortex.2014.07.019DOI Listing

Publication Analysis

Top Keywords

alzheimer's disease
8
anosognosia
6
anosognosia alzheimer's
4
disease diagnosis
4
diagnosis frequency
4
frequency mechanism
4
mechanism clinical
4
clinical correlates
4
correlates anosognosia
4
anosognosia large
4

Similar Publications

Background: The imbalance of glutamate (Glu) and gamma-aminobutyric acid (GABA) neurotransmitter system plays a crucial role in the pathogenesis of Alzheimer's disease (AD). Riluzole is a Glu modulator originally approved for amyotrophic lateral sclerosis that has shown potential neuroprotective effects in various neurodegenerative disorders. However, whether riluzole can improve Glu and GABA homeostasis in AD brain and its related mechanism of action remain unknown.

View Article and Find Full Text PDF

Upregulated astrocyte HDAC7 induces Alzheimer-like tau pathologies via deacetylating transcription factor-EB and inhibiting lysosome biogenesis.

Mol Neurodegener

January 2025

College of Life Sciences and Oceanography, Brain Disease and Big Data Research Institute, Shenzhen University, Shenzhen, 518060, Guangdong, China.

Background: Astrocytes, the most abundant glial cell type in the brain, will convert into the reactive state in response to proteotoxic stress such as tau accumulation, a characteristic feature of Alzheimer's disease (AD) and other tauopathies. The formation of reactive astrocytes is partially attributed to the disruption of autophagy lysosomal signaling, and inhibiting of some histone deacetylases (HDACs) has been demonstrated to reduce the molecular and functional characteristics of reactive astrocytes. However, the precise role of autophagy lysosomal signaling in astrocytes that regulates tau pathology remains unclear.

View Article and Find Full Text PDF

Remote, digital cognitive testing on an individual's own device provides the opportunity to deploy previously understudied but promising cognitive paradigms in preclinical Alzheimer's disease (AD). The Boston Remote Assessment for NeuroCognitive Health (BRANCH) captures a personalized learning curve for the same information presented over seven consecutive days. Here, we examined BRANCH multi-day learning curves (MDLCs) in 167 cognitively unimpaired older adults (age = 74.

View Article and Find Full Text PDF

A comprehensive genome-wide association study (GWAS) has validated the identification of the Plexin-A 4 (PLXNA4) gene as a novel susceptibility factor for Alzheimer's disease (AD). Nonetheless, the precise role of PLXNA4 gene polymorphisms in the pathophysiology of AD remains to be established. Consequently, this study is aimed at exploring the relationship between PLXNA4 gene polymorphisms and neuroimaging phenotypes intimately linked to AD.

View Article and Find Full Text PDF

Alzheimer's disease (AD), a prevalent neurodegenerative disorder, is characterized by mitochondrial dysfunction and immune dysregulation. This study is aimed at developing a risk prediction model for AD by integrating multi-omics data and exploring the interplay between mitochondrial energy metabolism-related genes (MEMRGs) and immune cell dynamics. We integrated four GEO datasets (GSE132903, GSE29378, GSE33000, GSE5281) for differential gene expression analysis, functional enrichment, and weighted gene co-expression network analysis (WGCNA).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!