Evidence map›Paper›PMID 35128031›Full record

ArticleAlzheimer's & dementia (New York, N. Y.)2022

Reversing Alzheimer's disease dementia with clemastine, fingolimod, or rolipram, plus anti-amyloid therapy.

Jeffrey Fessel

Abstract read
In one paragraph

Article in Alzheimer's & dementia (New York, N. Y.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Reduced myelin contributes to cognitive impairment in patients with monogenic small vessel disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  5. Research progress on phosphodiesterase 4 inhibitors in central nervous system diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. AD and non-AD mediators of the pathway between the APOE genotype and cognition.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. 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

1 author.

Jeffrey FesselProfessor of Clinical Medicine, Emeritus, Department of Medicine University of California, San Francisco San Francisco California USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A few anti-amyloid trials offer a slight possibility of preventing progression of cognitive loss, but none has reversed the process. A possible reason is that amyloid may be necessary but insufficient in the pathogenesis of AD, and other causal factors may need addressing in addition to amyloid. It is argued here that drugs addressing myelination and synaptogenesis are the optimum partners for anti-amyloid drugs, since there is much evidence that early in the process that leads to AD, both neural circuits and synaptic activity are dysfunctional. Evidence to support this argument is presented. Evidence is also presented that clemastine, fingolimod, and rolipram, benefit both myelination and synaptogenesis. It is suggested that a regimen that includes one of them plus an anti-amyloid drug, could reverse AD.

Indexed as

anti‐amyloid compoundsclemastinefingolimodreversing Alzheimer's dementiarolipramsupporting drugs

Identifiers

PMID35128031
PMCPMC8804619

What OpenQuestion holds

Textmetadata
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.