Abstract
Amyloid plaques, one of the main hallmarks of Alzheimer's disease (AD), are classified into diffuse (associated with cognitive impairment) and dense-core types (a common finding in brains of people without Alzheimer's disease (non-AD) and without impaired cognitive function) based on their morphology. We tried to determine the usability of gray-level co-occurrence matrix (GLCM) texture parameters of homogeneity and heterogeneity for the differentiation of amyloid plaque images obtained from AD and non-AD individuals. Images of amyloid-β (Aβ) immunostained brain tissue samples were obtained from the Aging, Dementia and Traumatic Brain Injury Project. A total of 1,039 plaques were isolated from different brain regions of 69 AD and non-AD individuals and used for further GLCM analysis. Images of Aβ stained plaques show higher values of heterogeneity parameters and lower values of homogeneity parameters in AD patients, and vice versa in non-AD patients. Additionally, GLCM analysis shows differences in Aβ plaque texture between different brain regions in non-AD patients and correlates with variables that characterize patient's dementia status. The present study shows that GLCM texture analysis is an efficient method to discriminate between different types of amyloid plaques based on their morphology and thus can prove as a valuable tool in the neuropathological investigation of dementia.
Highlights
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the presence of neurofibrillary tangles and amyloid plaques, which represent the histopathological hallmark of the disease (Perl, 2010)
Since the plaque formation and structure can potentially be influenced by the presence of Traumatic Brain Injury (TBI) and apolipoprotein E (ApoE)-ε4, we aimed to explore the influence of these two well-known AD risk factors in our sample group
Data exploration with three-way analysis of variance (ANOVA) shows no significant differences for ASM (F = 0.534, p > 0.05), inverse difference moment (IDM) (F = 0.351, p > 0.05), COR (F = 1.307, p > 0.05), CON (F = 0.574, p > 0.05), and ENT (F = 0.399, p > 0.05), which indicates a lack of patient group–TBI–ApoE-ε4 status interaction
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the presence of neurofibrillary tangles and amyloid plaques, which represent the histopathological hallmark of the disease (Perl, 2010). The two main findings that are inconsistent with the amyloid hypothesis are (1) the existence of amyloid plaques in brains of people without cognitive impairment and (2) the small amyloid plaque burden in a number of diagnosed AD patients (Edison et al, 2007). These plaques can be morphologically classified into diffuse and dense-core types based on their morphology and staining with Thioflavin-S or. Dense-core plaques cause neuron damage and subsequent microglia activation and are associated with cognitive impairment in AD patients. There is a need to properly distinguish between these two types of morphologically different plaques (Serrano-Pozo et al, 2011)
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