Risk factors for Alzheimer’s disease

Armstrong, Richard A.

doi:10.5114/fn.2019.85929

Cited by 367 publications

(305 citation statements)

References 182 publications

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“…Aβ deposits were more likely to be distributed across all cortical layers in AD and especially in CTE. AD and CTE are both tauopathies, but CTE is associated specifically with TBI [30,34,44,[51][52][53]62] while the cause of sporadic AD is likely to be more complex [11], identifying this disorder as having the most widespread laminar degeneration among those studied. The distribution of the classic Aβ deposits may be of particular significance in CTE as it could reflect blood vessel damage [5].…”

Section: Discussionmentioning

confidence: 99%

Cortical laminar distribution of β-amyloid deposits in five neurodegenerative disorders

Armstrong

2020

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Alzheimer's disease neuropathologic change (ADNC) in the form of β-amyloid (Aβ) deposits occurs not only in Alzheimer's disease (AD) and Down's syndrome (DS) but also as a 'co-pathology' in several disorders including dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), and chronic traumatic encephalopathy (CTE). To determine whether cortical laminar degeneration, as measured by Aβ deposition, is similar in different disorders, changes in density of the diffuse, primitive, and classic morphological subtypes of Aβ deposit were studied across all cortical layers in the frontal and temporal cortex in AD, DS, DLB, CBD, and CTE using quantitative analysis and polynomial curve fitting. In AD, CTE, and DLB, the diffuse Aβ deposits were distributed most frequently in the upper cortical layers, distribution being more variable in DS and CBD. In all disorders, the primitive Aβ deposits were distributed primarily in the upper layers, but in DLB, a bimodal distribution with peaks of density in upper and lower layers was evident in some gyri. The distribution of the classic deposits varied both within and among disorders. The many similarities in laminar distribution among disorders suggest common patterns of cortical degeneration. Where differences occur, they may reflect variations in the 'prion-like' propagation of Aβ along anatomical pathways in the different disorders.

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Section: Discussionmentioning

confidence: 99%

Cortical laminar distribution of β-amyloid deposits in five neurodegenerative disorders

Armstrong

2020

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“…3 In this regard, individual life style factors, environmental stress and resultant 'allostatic load' has been suggested as a major influencing factors in the disease trajectory of AD. 4 In line with this stance, recent major trials reported significant benefits of lifestyle interventions in those with high risk of AD. 5 Among many lifestyle and nonpharmacological interventions frequently discussed, 6 physical exercise is increasingly accentuated as a potential therapeutic strategy for AD, 7 with its beneficial effects on mitochondrial function, brain plasticity, neurogenesis and cerebral blood flow.…”

Section: Introductionmentioning

confidence: 86%

Effects of Moderate Intensity Exercise on the Cortical Thickness and Subcortical Volumes of Preclinical Alzheimer’s Disease Patients: A Pilot Study

Wang

Kim

et al. 2020

Psychiatry Investig

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Objective We aimed to explore the impact of moderate intensity exercise on the cortical thickness and subcortical volumes of preclinical Alzheimer’s disease (AD) patients.Methods Sixty-three preclinical AD patients with magnetic resonance imaging (MRI) and 18-florbetaben positron emission tomography (PET) data were enrolled in the study. Information on demographic characteristics, cognitive battery scores, self-reported exercise habits were attained. Structural magnetic resonance images were analyzed and processed using Freesurfer v6.0.Results Compared to Exercise group, Non-Exercise group demonstrated reduced cortical thickness in left parstriangularis, rostral middle frontal, entorhinal, superior frontal, lingual, superior parietal, lateral occipital, inferior parietal gyrus, temporal pole, precuneus, insula, fusiform gyrus, right precuneus, superiorparietal, lateral orbitofrontal, rostral middle frontal, medial orbitofrontal, superior frontal, lingual, middle temporal gyrus, insula, supramarginal, parahippocampal, paracentral gyrus. Volumes of right thalamus, caudate, putamen, pallidum, hippocampus, amygdala were also reduced in Non-Exercise group.Conclusion Moderate intensity exercise affects cortical and subcortical structures in preclinical AD patients. Thus, physical exercise has a potential to be an effective intervention to prevent future cognitive decline in those at high risk of AD.

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“…Among the genetic risk factors, the presence of mutations on the Apolipoprotein E (APOE) gene correlates with a high probability of developing SAD [14,15]. The APOE gene has three variants, namely ε2, ε3, and ε4 that have different roles in AD pathogenesis.…”

Section: Sporadic Form Of Alzheimer's Diseasementioning

confidence: 99%

The Other Side of Alzheimer’s Disease: Influence of Metabolic Disorder Features for Novel Diagnostic Biomarkers

Argentati

Tortorella

Bazzucchi

et al. 2020

JPM

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Nowadays, the amyloid cascade hypothesis is the dominant model to explain Alzheimer’s disease (AD) pathogenesis. By this hypothesis, the inherited genetic form of AD is discriminated from the sporadic form of AD (SAD) that accounts for 85–90% of total patients. The cause of SAD is still unclear, but several studies have shed light on the involvement of environmental factors and multiple susceptibility genes, such as Apolipoprotein E and other genetic risk factors, which are key mediators in different metabolic pathways (e.g., glucose metabolism, lipid metabolism, energetic metabolism, and inflammation). Furthermore, growing clinical evidence in AD patients highlighted the presence of affected systemic organs and blood similarly to the brain. Collectively, these findings revise the canonical understating of AD pathogenesis and suggest that AD has metabolic disorder features. This review will focus on AD as a metabolic disorder and highlight the contribution of this novel understanding on the identification of new biomarkers for improving an early AD diagnosis.

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Risk factors for Alzheimer’s disease

Cited by 367 publications

References 182 publications

Cortical laminar distribution of β-amyloid deposits in five neurodegenerative disorders

Cortical laminar distribution of β-amyloid deposits in five neurodegenerative disorders

Effects of Moderate Intensity Exercise on the Cortical Thickness and Subcortical Volumes of Preclinical Alzheimer’s Disease Patients: A Pilot Study

The Other Side of Alzheimer’s Disease: Influence of Metabolic Disorder Features for Novel Diagnostic Biomarkers

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