Evidence map›Paper›PMID 42358231›Full record

ReviewDegenerative neurological and neuromuscular disease2026

Spermidine in Alzheimer's Disease: Evidence from Animal Models and Human Studies.

Francesco Angelucci, Jiří Cerman, Jana Amlerova, Katerina Sheardova, Jan Pavlik, Jakub Hort

Abstract readReview
In one paragraph

Review in Degenerative neurological and neuromuscular disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Francesco AngelucciDepartment of Neurology, Second Faculty of Medicine, Charles University, Motol and Homolka University Hospital, Prague, Czech Republic.
Jiří CermanDepartment of Neurology, Second Faculty of Medicine, Charles University, Motol and Homolka University Hospital, Prague, Czech Republic.ORCID 0000-0003-1135-6865
Jana AmlerovaDepartment of Neurology, Second Faculty of Medicine, Charles University, Motol and Homolka University Hospital, Prague, Czech Republic.
Katerina SheardovaInternational Clinical Research Center, St. Anne's University Hospital Brno, Brno, Czech Republic.
Jan PavlikAlzheimerChain Foundation, Prague, Czech Republic.
Jakub HortDepartment of Neurology, Second Faculty of Medicine, Charles University, Motol and Homolka University Hospital, Prague, Czech Republic.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spermidine is a naturally occurring polyamine involved in multiple cellular processes, including growth regulation, protein translation, and autophagy. Increasing attention has been devoted to its potential neuroprotective effects, particularly in Alzheimer's disease (AD), a neurodegenerative disorder characterized by β-amyloid and phosphorylated tau accumulation, synaptic dysfunction, and progressive neuronal loss. In this narrative review, we examine potential mechanisms through which spermidine may influence AD pathophysiology and summarize available preclinical and clinical evidence. Preclinical studies indicate that spermidine induces autophagy, a key cellular clearance pathway responsible for removing damaged organelles and aggregated proteins. Because impaired neuronal autophagy contributes to the accumulation of β-amyloid and tau in AD, increasing intracellular spermidine levels may enhance the degradation of these toxic species. In addition, spermidine exhibits anti-inflammatory and antioxidant properties, attenuates microglial activation, and supports mitochondrial function. In animal models of AD and brain aging, spermidine administration has been associated with improvements in cognitive performance and synaptic function. However, human clinical evidence remains limited and largely inconclusive. Observational studies suggest associations between higher dietary spermidine intake and better cognitive outcomes, but do not establish causality. Randomized clinical trials to date are few, include small and heterogeneous populations, and have not demonstrated consistent effects on primary cognitive endpoints. Overall, spermidine represents a biologically plausible modulator of pathways relevant to neurodegeneration, but translation of preclinical findings into clinical benefit remains uncertain. Current evidence is insufficient to support its use as a therapeutic or preventive intervention in AD, and further well-designed clinical studies are required to clarify its efficacy and mechanisms of action.

Indexed as

Alzheimer’s diseaseautophagycognitiondietneuroinflammationspermidine

Identifiers

PMID42358231
PMCPMC13292852

What Socratic holds

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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 Socratic graph.