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Comment
. 2013 Mar 1;73(5):393-5.
doi: 10.1016/j.biopsych.2013.01.013.

CR1 and the "vanishing amyloid" hypothesis of Alzheimer's disease

Sam Gandy  1 , Vahram Haroutunian, Steven T DeKosky, Mary Sano, Eric E Schadt
Affiliations
Comment

CR1 and the "vanishing amyloid" hypothesis of Alzheimer's disease

Sam Gandy et al. Biol Psychiatry. .
No abstract available

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Conflict of interest statement

VH reports no biomedical financial interests or potential conflicts of interest.

Figures

Figure 1
Figure 1
A model of Alzheimer’s disease as a feed-forward cycle of neuropathology and immunoinflammatory pathology. (Reproduced with permission from Neumann and Takahashi [4]).
Figure 2
Figure 2
Arctic APP mutations are associated with reduced 11C-PiB retention. Transaxial sections of individual magnetic resonance imaging (upper row), Pittsburgh compound B (PiB) (middle row), and 18F-fluorodeoxyglucose (FDG) positron emission tomography (lower row) scans of all participants. Images of patients with sporadic Alzheimer’s disease (sAD) and healthy controls (HCs) are mean images. The Arctic APP (APParc) mutation carriers APParc-1 and APParc-2 showed very low cortical PiB retention, comparable with the five noncarriers APParc 3–7 and HCs. APParc-1 revealed globally decreased glucose metabolism and brain atrophy, and APParc-2 regionally decreased glucose metabolism. MCI, mild cognitive impairment. (Reproduced with permission from Schöll et al. [7]).
Figure 3
Figure 3
Inflammatome gene regulatory (Bayesian) network enriched for AD genes identified and highly replicated in genetic studies. (A) A probabilistic causal network constructed from human omental adipose tissue collected in a cohort of morbidly obese patients (13). The nodes in the network are gene expression traits monitored in the omental adipose tissue from this cohort. The directed links between the nodes are derived via a Bayesian network reconstruction algorithm that leverages DNA variation as a systematic perturbation source to resolve causality (14). The pink nodes highlighted in this network are the inflammatome signature genes we have previously identified as strongly causally associated with a number of diseases (–15). (B) A zoomed-in view of the subnetwork highlighted in panel (A) by the pink nodes. This inflammatome-based network is enriched for inflammatory and immune response gene ontology categories (color-coded pathways are indicated; all enrichments are significant at a 1% false discovery rate). In addition, genes previously identified in genetic studies and extensively replicated as associated with AD are represented in this network, including the genes highlighted: TREM2, CR1, CD33, MS4A4A, MS4A6A, and HCK
See this image and copyright information in PMC

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References

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