Biological process categories overrepresented by the genes related to AD neuropathology (npADGs).

<p>Biological process categories significantly overrepresented by npADGs (P<0.05, Fisher’s exact test). Other similar significant categories are not included to reduce redundancy.</p

Interaction networks of the significant genes and their interacting partners.

<p>(<b>A</b>) Shown are the genes (color nodes) that have, as a function of presence (CP-AD + P-AD) or absence (N) of AD pathology, significantly different correlation of co-expression with their partners. Green nodes indicate genes that are significantly differently expressed between patient groups, while light blue nodes indicate genes that are not significantly differently expressed. Edge colors represent the correlation between a gene and each of its partners. (<b>B</b>) <i>MYC</i> and its interacting partners. Note that the significant genes and their partners form an interconnected network, and despite the interactions involving <i>MYC</i> are not significantly altered, it has a lot of connections, playing an important role as a hub gene. CP-AD, clinic-pathological Alzheimer’s disease; P-AD, pathological/preclinical Alzheimer’s disease; N, normal samples (controls).</p

Hypothetical model of the gene expression alterations related to neuropathology and clinical manifestation of Alzheimer’s disease (AD).

<p>Gene expression profile changes related to AD pathology are implicated with energy metabolism, oxidative stress, DNA damage and transcriptional regulation. Once established of significant AD pathology, some genes involved with synaptic plasticity, and cell cycle appear to be involved with the clinical outcome of the illness and might represent the molecular mechanisms that underlie the cognitive reserve. CP-AD, clinic-pathological Alzheimer’s disease; P-AD, pathological/preclinical Alzheimer’s disease.</p

Summary of selected cases.

<p>Subjects were divided in three groups according to neuropathological and clinical criteria: clinic-pathological Alzheimer’s disease (CP-AD), pathological/preclinical Alzheimer’s disease (P-AD), and normal older individuals (N). Sample ID, sample identification; Age, age at death in years; F, female; M, male; Braak, Braak stage; CERAD, Consortium to Establish a Registry for Alzheimeŕs Disease score; CDR, Clinical Dementia Ratio score; PMI, post-mortem interval in hours.</p

Hierarchical clustering analysis of CP-AD, P-AD and N samples.

<p>Hierarchical clustering was performed by using the expression values from the genes related to AD neuropathology with <i>P</i>≤0.005 (47 transcripts). Each row represents a single gene and each column a sample (dark blue, CP-AD samples; light blue, P-AD samples; yellow, N samples). Red indicates upregulation, green indicates downregulation, and black indicates no change in expression level comparing to reference sample. Cluster support was given by Bootstrap technic (black, 100% of support; grey, 90–100%; blue, 80–90%; green, 70–80%; light yellow, 60–70%; dark yellow, 50–60%; magenta, 0–50%, red, 0%). CP-AD, clinic-pathological Alzheimer’s disease; P-AD, pathological/preclinical Alzheimer’s disease; N, normal samples (controls).</p

Multivariate (three-gene) discriminators for Alzheimer’s disease (AD) classification.

<p>(<b>A</b>) Discriminator of CP-AD samples (blue) and P-AD samples (red) using the expression values of <i>PTPRN</i>, <i>ULK2</i>, and <i>HES1</i> genes. (<b>B</b>) Discriminator of CP-AD samples (blue) and P-AD samples (red) using the expression values of <i>CAPRIN1</i>, <i>ULK2</i>, and <i>RFC2</i> genes. CP-AD, clinic-pathological Alzheimer’s disease; P-AD, pathological/preclinical Alzheimer’s disease.</p

Association of visceral fat with the degree and extension of atherosclerosis (n = 240).

<p>Association of visceral fat with the degree and extension of atherosclerosis (n = 240).</p

Average number of cells in the olfactory bulb of men and women.

<p>Blue bars indicate the mean number of cells in males, pink bars for females. Significant differences were found for the total number of cells, as well as for the number of neurons and non-neuronal cells. In all cases, women outnumbered men. Error bars indicate standard deviation. * p<0.05; ** p<0.01.</p

Morphometric measurements of systemic atherosclerosis and visceral fat: Evidence from an autopsy study - Fig 5

<p><b>Predicted values of the number of plaques in (A) coronary and (B) cerebral arteries according to the amount of abdominal visceral fat, and in the (C) coronary and (D) cerebral arteries according to the amount of pericardial fat for participants with 40 (blue line), 60 (green line), and 80 (red line) years old, using linear regression models adjusted for height, age, sex, smoking status, alcohol use, physical inactivity, hypertension, and diabetes mellitus, and including an interaction between age and abdominal visceral fat or pericardial fat</b>.</p

Association between visceral fat and atherosclerosis in different arterial sites, considering an interaction term between visceral fat and age (n = 240).

<p>Association between visceral fat and atherosclerosis in different arterial sites, considering an interaction term between visceral fat and age (n = 240).</p