Evidence map›Paper›PMID 24614496›Full record

ArticleMolecular psychiatry2015

Intraperitoneal injection of the pancreatic peptide amylin potently reduces behavioral impairment and brain amyloid pathology in murine models of Alzheimer's disease.

H Zhu, X Wang, M Wallack, H Li, I Carreras, A Dedeoglu, J-Y Hur, H Zheng, H Li, R Fine and 5 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Amylin: From Mode of Action to Future Clinical Potential in Diabetes and Obesity.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
    Review
  4. Review
  5. Article
  6. Mechanism of Metal Complexes in Alzheimer's Disease.International journal of molecular sciences · 2024
    Review
  7. A small TAT-TrkB peptide prevents BDNF receptor cleavage and restores synaptic physiology in Alzheimer's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
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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

15 authors at 4 institutions in 1 country.

H ZhuDepartment of Pharmacology and Experimental Therapeutics, Boston University Medical Campus, Boston, MA, USA.
X WangDepartment of Pharmacology and Experimental Therapeutics, Boston University Medical Campus, Boston, MA, USA.
M WallackDepartment of Pharmacology and Experimental Therapeutics, Boston University Medical Campus, Boston, MA, USA.
H LiDepartment of Pharmacology and Experimental Therapeutics, Boston University Medical Campus, Boston, MA, USA.ORCID 0000000249521734
I Carreras1] Department of Neurology, Boston University Medical Campus, Boston, MA, USA [2] Alzheimer's Disease Center, Boston University Medical Campus, Boston, MA, USA.
A Dedeoglu1] Department of Neurology, Boston University Medical Campus, Boston, MA, USA [2] Alzheimer's Disease Center, Boston University Medical Campus, Boston, MA, USA.
J-Y HurMemorial Sloan-Kettering Institute, New York, NY, USA.
H ZhengDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
H LiDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
R Fine1] Alzheimer's Disease Center, Boston University Medical Campus, Boston, MA, USA [2] ENRM VA Medical Center, Bedford, MA, USA.
M MwamburiDepartment of Public Health and Family Medicine, Tufts University, Boston, MA, USA.
X Sun1] Department of Neurology, Boston University Medical Campus, Boston, MA, USA [2] Alzheimer's Disease Center, Boston University Medical Campus, Boston, MA, USA.
N Kowall1] Department of Neurology, Boston University Medical Campus, Boston, MA, USA [2] Alzheimer's Disease Center, Boston University Medical Campus, Boston, MA, USA.
R A Stern1] Department of Neurology, Boston University Medical Campus, Boston, MA, USA [2] Alzheimer's Disease Center, Boston University Medical Campus, Boston, MA, USA [3] Department of Neural Surgery, Boston University Medical Campus, Boston, MA, USA.
W Q Qiu1] Department of Pharmacology and Experimental Therapeutics, Boston University Medical Campus, Boston, MA, USA [2] Alzheimer's Disease Center, Boston University Medical Campus, Boston, MA, USA [3] Department of Psychiatry, Boston University Medical Campus, Boston, MA, USA.
Boston University · USBaylor College of Medicine · USMemorial Sloan Kettering Cancer Center · USTufts University · US

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
Plasma Amyloid-beta Peptides, Depression and Alzheimer's Disease in the HomeboundR01AG031171 · NIA · TUFTS MEDICAL CENTER · PI QIU, WEI QIAO WENDY · 2009 to 2013
$2.0M
Midcareer Investigator Award in Amylin, Cognition, and Alzheimer's DiseaseK24AG050842 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI QIU, WEI QIAO WENDY · 2015 to 2019
$850k
Insulin, Cognitive Impairment and Alzheimer's DiseaseK23AG022476 · NIA · TUFTS MEDICAL CENTER · PI QIU, WEI QIAO WENDY · 2003 to 2007
$658k
Amylin as a Diagnostic Test and Potential Treatment for Alzheimers DiseaseR21AG045757 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI QIU, WEI QIAO WENDY · 2014 to 2015
$444k
NIA NIH HHS AG-022476NIA NIH HHS K23 AG022476NIA NIH HHS K24 AG050842NIA NIH HHS P30 AG013846NIA NIH HHS P30 AG13864NIA NIH HHS R01 AG031171NIA NIH HHS R21 AG045757
6 · The paper itself

Abstract

Amylin, a pancreatic peptide, and amyloid-beta peptides (Aβ), a major component of Alzheimer's disease (AD) brain, share similar β-sheet secondary structures, but it is not known whether pancreatic amylin affects amyloid pathogenesis in the AD brain. Using AD mouse models, we investigated the effects of amylin and its clinical analog, pramlintide, on AD pathogenesis. Surprisingly, chronic intraperitoneal (i.p.) injection of AD animals with either amylin or pramlintide reduces the amyloid burden as well as lowers the concentrations of Aβ in the brain. These treatments significantly improve their learning and memory assessed by two behavioral tests, Y maze and Morris water maze. Both amylin and pramlintide treatments increase the concentrations of Aβ1-42 in cerebral spinal fluid (CSF). A single i.p. injection of either peptide also induces a surge of Aβ in the serum, the magnitude of which is proportionate to the amount of Aβ in brain tissue. One intracerebroventricular injection of amylin induces a more significant surge in serum Aβ than one i.p. injection of the peptide. In 330 human plasma samples, a positive association between amylin and Aβ1-42 as well as Aβ1-40 is found only in patients with AD or amnestic mild cognitive impairment. As amylin readily crosses the blood-brain barrier, our study demonstrates that peripheral amylin's action on the central nervous system results in translocation of Aβ from the brain into the CSF and blood that could be an explanation for a positive relationship between amylin and Aβ in blood. As naturally occurring amylin may play a role in regulating Aβ in brain, amylin class peptides may provide a new avenue for both treatment and diagnosis of AD.

Indexed as

Alzheimer DiseaseAmylin Receptor AgonistsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesDisease Models, AnimalFemaleGene Expression RegulationHumansIslet Amyloid PolypeptideMaleMaze LearningMental DisordersMiceAmylin Receptor AgonistsAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Amyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBace1 protein, mouseIslet Amyloid PolypeptidePeptide FragmentsPresenilin-1PSEN1 protein, human

Identifiers

PMID24614496
PMCPMC4161670
OpenAlexW2065714314

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.