Evidence map›Paper›PMID 23794448›Full record

ArticleAnnals of neurology2013

Amylin deposition in the brain: A second amyloid in Alzheimer disease?

Kaleena Jackson, Gustavo A Barisone, Elva Diaz, Lee-way Jin, Charles DeCarli, Florin Despa

Open access · greenAbstract read
In one paragraph

Article in Annals of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
215citing papers in PubMed, 2 pooled it
13.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

215 citing papers in PubMed, 2 syntheses or guidelines pooled it, 334 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Diabetes-Associated Cognitive Impairment: Pathophysiology and Emerging Therapies.Annals of clinical and translational neurology · 2026
    Review
  4. Review
  5. Diabetes, hyperglycemia, and ATN blood biomarkers in Hispanic/Latino populations: SOL-INCA study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  7. Article
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  9. Mammals that can develop type 2 diabetes have a similarly structured β-sheet amyloid oligomer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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155 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Kaleena JacksonDepartment of Pharmacology, University of California, Davis, Davis, CA.
Gustavo A Barisone
Elva Diaz
Lee-way Jin
Charles DeCarli
Florin Despa
University of California, Davis · USUniversity of California Davis Medical Center · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
NRF2 Anti-Oxidant Systems and White Matter HyperintensitiesR01AG042292 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DECARLI, CHARLES, SHARP, FRANK R · 2013 to 2017
$3.0M
Hyperamylinemia in Diabetic Heart Disease: Mechanisms, Responses, and PreventionR01HL118474 · NHLBI · UNIVERSITY OF KENTUCKY · PI DESPA, FLORIN · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL118474NIA NIH HHS P30 AG010129NIA NIH HHS P30AG010129NIA NIH HHS R01 AG042292
6 · The paper itself

Abstract

objectiveHyperamylinemia, a common pancreatic disorder in obese and insulin-resistant patients, is known to cause amylin oligomerization and cytotoxicity in pancreatic islets, leading to β-cell mass depletion and development of type 2 diabetes. Recent data has revealed that hyperamylinemia also affects the vascular system, heart, and kidneys. We therefore hypothesized that oligomerized amylin might accumulate in the cerebrovascular system and brain parenchyma of diabetic patients.

methodsAmylin accumulation in the brain of diabetic patients with vascular dementia or Alzheimer disease (AD), nondiabetic patients with AD, and age-matched healthy controls was assessed by quantitative real time polymerase chain reaction, immunohistochemistry, Western blot, and enzyme-linked immunosorbent assay.

resultsAmylin oligomers and plaques were identified in the temporal lobe gray matter from diabetic patients, but not controls. In addition, extensive amylin deposition was found in blood vessels and perivascular spaces. Intriguingly, amylin deposition was also detected in blood vessels and brain parenchyma of patients with late onset AD without clinically apparent diabetes. Mixed amylin and amyloid β (Aβ) deposits were occasionally observed. However, amylin accumulation leads to amyloid formation independent of Aβ deposition. Tissues infiltrated by amylin showed increased interstitial space, vacuolation, spongiform change, and capillaries bent at amylin accumulation sites. Unlike the pancreas, there was no evidence of amylin synthesis in the brain.

interpretationMetabolic disorders and aging promote accumulation of amylin amyloid in the cerebrovascular system and gray matter, altering microvasculature and tissue structure. Amylin amyloid formation in the wall of cerebral blood vessels may also induce failure of elimination of Aβ from the brain, thus contributing to the etiology of AD.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesBrainDiabetic AngiopathiesFemaleHumansIslet Amyloid PolypeptideMaleRNA, MessengerAmyloid beta-PeptidesIslet Amyloid PolypeptideRNA, Messenger

Identifiers

PMID23794448
PMCPMC3818462
OpenAlexW1837066325

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.