Evidence mapPaperPMID 41198597Full record

ReviewJournal of internal medicine2026

Bioenergetics and lipid metabolism in Alzheimer's disease: From cell biology to systemic health.

Silvia Maioli, Ivan Nalvarte, Maria Ankarcrona, Marianne Schultzberg, Kristen L Zuloaga, Julen Goikolea, Pieter Jelle Visser, Bart De Strooper, Bengt Winblad, Paola Pizzo and 3 more

Abstract readReview
In one paragraph

Review in Journal of internal medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Mitochondrial CaBiomolecules · 2026
    Review
  10. 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

13 authors.

Silvia MaioliDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
Ivan NalvarteDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0001-6828-2583
Maria AnkarcronaDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
Marianne SchultzbergDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
Kristen L ZuloagaDepartment of Neuroscience & Experimental Therapeutics, Albany Medical College, Albany, New York, USA.
Julen GoikoleaDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
Pieter Jelle VisserDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
Bart De StrooperLaboratory for Neurodegenerative Diseases, VIB-KU Leuven, and Leuven Brain Institute, Leuven, Belgium.
Bengt WinbladDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
Paola PizzoDepartment of Biomedical Sciences, University of Padua, Padua, Italy.
Pete A WilliamsDepartment of Clinical Neuroscience, Division of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet, Stockholm, Sweden.
Patricia Rodriguez-RodriguezDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.
Luana NaiaDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Stockholm, Sweden.ORCID https://orcid.org/0000-0002-0886-4634

Funding

Metabolic and Hormonal Mechanisms of VCIDR01NS110749 · ALBANY MEDICAL COLLEGE · 2025 to 2025
$814k
Cure Alzheimer's Fund (USA)Dementia FoundationEuropean Union, NextGeneration EUGun och Bertil Stohnes StiftelseItalian Ministry of Research, NRRP-National Recovery and Resilience Plan grant, National Centre of Research 'Development of gene therapy and drugs with RNA technology', spoke 3 'Neurodegenerative DiseasesItalian Ministry of University and Scientific Research PRIN2022943TH9Italian Ministry of University and Scientific Research PRIN P20225R4Y5King Gustaf V:s and Queen Victoria's Foundation, Gun och Bertil Stohnes Stiftelse, Stiftelsen Gamla TjänarinnorLeif Lundblad Family and othersMargaretha af Ugglas FoundationNational Institutes of Health (NIH) research NS110749NINDS NIH HHS R01 NS110749Strategic Research Program in Neuroscience-StratNeuroSwedish Alzheimer Foundation AF-1011030Swedish Alzheimer Foundation AF-1012350Swedish Research Council 2022-00799Swedish Research Council 2023-02054Swedish Research Council 2024-03440Swedish Research Council 2024-03577Swedish Research Council 2323-02503the Swedish Brain Foundation 2024-0287the Swedish Brain Foundation FO2024-0153-HK-50Ulla and Ingemar Dahlberg Foundation
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline. Although amyloid-β and tau pathologies remain central to our understanding of AD, growing evidence suggests that disrupted lipid metabolism and impaired bioenergetics are closely linked to these hallmark features. Genetic, lipidomic and functional studies point to alterations in cholesterol, phospholipids and polyunsaturated fatty acids, which can influence mitochondrial function, organelle communication and glial responses. These processes are further modulated by apolipoprotein E (APOE) genotype, sex differences and systemic metabolic states such as obesity and diabetes, contributing to neuroinflammation and cognitive decline. Although findings are sometimes conflicting, an emerging theme is that lipid and energy metabolisms are central to how genetic and environmental risk factors shape AD pathogenesis. This integrated perspective highlights lipid and bioenergetic pathways as promising therapeutic targets, where metabolic modulators, lipid-directed interventions and lifestyle strategies may complement amyloid-based therapies and offer opportunities for precision approaches, particularly in women and APOE ε4 carriers.

Indexed as

Alzheimer DiseaseEnergy MetabolismLipid MetabolismApolipoproteins EHumansMitochondriaApolipoproteins EAlzheimer's diseaselipid metabolismmitochondriasystemic metabolism

Identifiers

PMID41198597
PMCPMC12678226

What Socratic 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 Socratic graph.