Relationships between β-amyloid (Aβ) deposits and blood vessels in patients with sporadic and familial Alzheimer's disease

Armstrong, Richard A.; Cairns, Nigel J.; Patel, Ranish K.; Rossor, Martin N.

doi:10.1016/0304-3940(96)12525-8

Cited by 14 publications

(21 citation statements)

References 28 publications

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“…In addition, Akiyama et al [1] found that Aβ deposits accumulated vertically in columns, with blood vessels often occurring perpendicular to the column and penetrating its centre. Previous studies suggest, however, that although classic Aβ deposits are clustered around blood vessels in SAD [6], there are fewer spatial associations with blood vessels in FAD [7].…”

Section: Discussionmentioning

confidence: 82%

“…Hence, to label all types of plaque 7 µm coronal sections were immunolabelled with a rabbit polyclonal antibody (Gift of Prof. B.H. Anderton, Institute of Psychiatry, King's College London) raised to the 12-28 amino acid sequence of the Aβ protein and first used to identify Aβ deposit subtypes in Down's syndrome (DS) [50] but which also effectively distinguishes the major types of Aβ deposit in AD [4,6,7,10,50]. The antibody was used at a dilution of 1 in 1200 and the sections incubated at 4°C overnight.…”

Section: Tissue Preparationmentioning

confidence: 99%

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Original article Laminar distribution of β-amyloid (Aβ) peptide deposits in the frontal lobe in familial and sporadic Alzheimer’s disease

Armstrong¹

2015

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A b s t r a c t To determine whether genetic factors influence frontal lobe degeneration in Alzheimer's disease (AD), the laminar distributions of diffuse, primitive, and classic β-amyloid (Aβ) peptide deposits were compared in early-onset familial AD (EO-FAD) linked to mutations of the amyloid precursor protein (APP) or presenilin 1 (PSEN1) gene, late-onset familial AD (LO-FAD), and sporadic AD (SAD). The influence of apolipoprotein E (Apo E) genotype on laminar distribution was also studied. In the majority of FAD and SAD cases, maximum density of the diffuse and primitive Aβ deposits occurred in the upper cortical layers, whereas the distribution of the classic Aβ deposits was more variable, either occurring in the lower layers, or a double-peaked (bimodal) distribution was present, density peaks occurring in upper and lower layers. The cortical layer at which maximum density of Aβ deposits occurred and maximum density were similar in EO-FAD, LO-FAD and SAD. In addition, there were no significant differences in distributions in cases expressing

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Section: Discussionmentioning

confidence: 82%

Section: Tissue Preparationmentioning

confidence: 99%

Original article Laminar distribution of β-amyloid (Aβ) peptide deposits in the frontal lobe in familial and sporadic Alzheimer’s disease

Armstrong¹

2015

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“…Aß originating in blood vessel walls can develop into amyloid [93] which would support this hypothesis. However, this process is unlikely to explain the pathogenesis of most primitive plaques which are not correlated with blood vessels but could explain the pathogenesis of some classic plaques [89,94].…”

Section: Pathogenesis Of Aß Plaquesmentioning

confidence: 99%

“…2K). Different types of classic plaque have been observed in AD [3,57,88] which would also suggest that cored plaques could arise by different pathogenic processes [94].…”

Section: Pathogenesis Of Aß Plaquesmentioning

confidence: 99%

β-Amyloid Plaques: Stages in Life History or Independent Origin?

Armstrong

1998

Dement Geriatr Cogn Disord

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Several types of discrete β-amyloid (Aβ) deposit or senile plaque have been identified in the brains of individuals with Alzheimer’s disease and Down’s syndrome. The majority of these plaques can be classified into four morphological types: diffuse, primitive, classic and compact. Two hypotheses have been proposed to account for these plaques. Firstly, that the diffuse, primitive, classic and compact plaques develop in sequence and represent stages in the life history of a single plaque type. Secondly, that the different Aβ plaques develop independently and therefore, unique factors are involved in the formation of each type. To attempt to distinguish between these hypotheses, the morphology, ultrastructure, composition, and spatial distribution in the brain of the four types of plaque were compared. Although some primitive plaques may develop from diffuse plaques, the evidence suggests that a unique combination of factors is involved in the pathogenesis of each plaque type and, therefore, supports the hypothesis that the major types of Aβ plaque develop independently.

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“…The changes within the brain that accompany these symptoms are toxic proteins (amyloid beta -Aβ) referred to as 'tangles' and 'plaques' (Kennard, 2006). These pathological neurofibrillary tangles accumulate in the entorhinal cortex and hippocampus parts of the brain, used for short and long-term memory (Armstrong et al, 1996). Neuroscientists have researched that in order to keep the memory alive the communication between these two parts is essential, were any compromises often leads to memory disturbance and eventually memory loss (Braak and Braak, 1991).…”

Section: Alzheimer's Parkinson's Huntington's and Alsmentioning

confidence: 99%

A classifier fusion strategy to improve the early detection of neurodegenerative diseases

Iram

Fergus

Al‐Jumeily

et al. 2015

IJAISC

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People in developed countries are living longer, and this has resulted in the prevalence of age-related diseases like Alzheimer's and dementia. Many believe that the early detection of neurodegenerative diseases will provide a much more sustainable framework for dealing with age-related diseases in the future. This paper considers this idea and proposes a new classifier fusion strategy that combines classification algorithms and rules (voting, product, mean, median, maximum and minimum) to measure specific behaviours in people suffering with neurodegenerative diseases. More specifically, the fusion strategy analyses the stride-to-stride intervals in gait and its correlation with neurological functions. This approach is compared with base level classifiers (a single classification algorithm) using a set of feature vectors associated with gait patterns obtained from neurodegenerative patients and healthy people. The results show that the fusion strategy improves classification. Our experiments successfully show that a fusion strategy generates better results and classifies subjects more accurately than base level classifiers.Keywords: combining classifiers; pattern recognition; behaviour classification; machine learning; Huntington's disease; Parkinson's disease amyotrophic lateral sclerosis; ALS; movement signals; artificial intelligence.Reference to this paper should be made as follows: Iram, S., Fergus, P., Al-Jumeily, D., Hussain, A. and Randles, M. (2015) 'A classifier fusion strategy to improve the early detection of neurodegenerative diseases', Int.

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Relationships between β-amyloid (Aβ) deposits and blood vessels in patients with sporadic and familial Alzheimer's disease

Cited by 14 publications

References 28 publications

Original article Laminar distribution of β-amyloid (Aβ) peptide deposits in the frontal lobe in familial and sporadic Alzheimer’s disease

Original article Laminar distribution of β-amyloid (Aβ) peptide deposits in the frontal lobe in familial and sporadic Alzheimer’s disease

β-Amyloid Plaques: Stages in Life History or Independent Origin?

A classifier fusion strategy to improve the early detection of neurodegenerative diseases

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