Evidence map›Paper›PMID 38363009›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024

Tracing synaptic loss in Alzheimer's brain with SV2A PET-tracer UCB-J.

Amit Kumar, Miriam Scarpa, Agneta Nordberg

Open access · hybridAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
10.8field-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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  14. Imaging Synaptic Density in Aging and Alzheimer Disease with [Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025
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  18. Observational
  19. SV2A PET shows hippocampal synaptic loss in cognitively unimpaired APOE ε4/ε4 homozygotes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  20. Review
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

3 authors at 2 institutions in 1 country.

Amit KumarDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Miriam ScarpaDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Agneta NordbergDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

Research Education ComponentP30AG010133 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SAYKIN, ANDREW J · 1991 to 2020
$37.3M
Research Education ComponentP30AG072976 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI ANDREW J SAYKIN · 2021 to 2026
$24.1M
Alzheimer's Association -21-848395NIA NIH HHS P30 AG010133NIA NIH HHS P30 AG072976
6 · The paper itself

Abstract

introductionSynaptic loss is an early prominent feature of Alzheimer's disease (AD). The recently developed novel synaptic vesicle 2A protein (SV2A) PET-tracer UCB-J has shown great promise in tracking synaptic loss in AD. However, there have been discrepancies between the findings and a lack of mechanistic insight.

methodsHere we report the first extensive pre-clinical validation studies for UCB-J in control (CN; n = 11) and AD (n = 11) brains using a multidimensional approach of post-mortem brain imaging techniques, radioligand binding, and biochemical studies. RESULTS AND DISCUSSION: We demonstrate that UCB-J could target SV2A protein with high specificity and depict synaptic loss at synaptosome levels in AD brain regions compared to CNs. UCB-J showed highest synaptic loss in AD hippocampus followed in descending order by frontal cortex, temporal cortex, parietal cortex, and cerebellum. HIGHLIGHTS: Synaptic positron emission tomography (PET)-tracer UCB-J could target synaptic vesicle 2A protein (SV2A) with high specificity in Alzheimer's disease (AD) and control brains. Synaptic PET-tracer UCB-J could depict synaptic loss at synaptosome levels in AD brain regions compared to control. Potential off-target interaction of UCB-J with phosphorylated tau (p-tau) species at cellular/subcellular levels could have subsequent clinical implications for imaging studies, warranting further investigations.

Indexed as

Alzheimer DiseaseBrainCerebellumHumansMembrane GlycoproteinsNerve Tissue ProteinsPositron-Emission TomographySynaptic VesiclesMembrane GlycoproteinsNerve Tissue ProteinsSV2A protein, humanAlzheimer's diseasebiomarkersPET ligandsSV2Asynaptic lossUCB‐J

Identifiers

PMID38363009
PMCPMC11032538
OpenAlexW4391884316

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.