Evidence map›Paper›PMID 41152198›Full record

ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Glymphatic and meningeal lymphatic dysfunction in Alzheimer's disease: Mechanisms and therapeutic perspectives.

Jiangwei Ding, Chengbin Zhao, Xiaoyan Hao, Hongliang Jiao

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Choroid plexus remodeling linked to impaired CSF-mediated clearance and Alzheimer's disease progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  6. Reconstructing cerebral lymphatic clearance: an emerging target in the Alzheimer's disease therapeutic pipeline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Glymphatic and meningeal lymphatic dysfunction in Alzheimer's disease: Mechanisms and therapeutic perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  19. Article
  20. Article
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

4 authors.

Jiangwei DingDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan, China.
Chengbin ZhaoDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan, China.
Xiaoyan HaoDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan, China.
Hongliang JiaoDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City, Henan, China.

Funding

the Henan Provincial Medical Science and Technology Research Project LHGJ20230249
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (Aβ) deposition and tau pathology. Although disease-modifying therapies, such as anti-Aβ monoclonal antibodies, have been approved, their clinical efficacy remains modest and accompanied by substantial safety concerns. The glymphatic system, which is a brain-wide waste clearance network mediated by cerebrospinal fluid-interstitial fluid exchange, is critical in AD pathogenesis. Glymphatic dysfunction promotes Aβ and tau accumulation, neuroinflammation, and vascular impairment, forming a vicious cycle that drives neurodegeneration. This review elucidates the anatomical and physiological basis of the glymphatic system, its role in AD progression, and novel therapeutic strategies targeting glymphatic enhancement. Emerging interventions, including aquaporin-4 (AQP4) modulation, meningeal lymphatic regeneration, cervical deep lymphaticovenous anastomosis, and nonpharmacological approaches, are also discussed for their potential to shift AD therapeutics from symptom management to disease modification. HIGHLIGHTS: Glymphatic dysfunction drives Alzheimer's disease (AD) pathogenesis. Meningeal lymphatic decline with aging. Cervical lymphaticovenous anastomosis (LVA) as novel new intervention method for patients with AD The apolipoprotein E (APOE) ε4 allele disrupts meningeal lymphatic function, increasing AD risk via amyloid-β (Aβ) clearance deficits. Diffusion tensor imaging along the perivascular space (DTI-ALPS) and dynamic magnetic resonance imaging (MRI) enable early detection of glymphatic dysfunction, guiding pre-symptomatic AD interventions. Sleep and arterial pulsatility critically regulate glymphatic efficiency, offering non-pharmacological therapeutic avenues.

Indexed as

Alzheimer DiseaseGlymphatic SystemMeningesAmyloid beta-PeptidesHumansAmyloid beta-PeptidesAlzheimer's diseaseglymphatic systemlymphatic–venous anastomosisneuroinflammationsleepβ‐amyloid clearance

Identifiers

PMID41152198
PMCPMC12568399

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.