Evidence map›Paper›PMID 24418409›Full record

ReviewBiochemical pharmacology2014

Alzheimer disease therapeutics: focus on the disease and not just plaques and tangles.

Khalid Iqbal, Fei Liu, Cheng-Xin Gong

Abstract readReview
In one paragraph

Review in Biochemical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 107 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  8. Article
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  11. Article
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  14. Article
  15. Microtubule Dysfunction: A Common Feature of Neurodegenerative Diseases.International journal of molecular sciences · 2020
    Review
  16. Overdosing on iron: Elevated iron and degenerative brain disorders.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  17. Article
  18. Tau Protein and Its Role in Blood-Brain Barrier Dysfunction.Frontiers in molecular neuroscience · 2020
    Review
  19. 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 1 institution in 1 country.

Khalid IqbalDepartment of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA. Electronic address: khalid.iqbal.ibr@gmail.com.
Fei LiuDepartment of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA.
Cheng-Xin GongDepartment of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA.
New York State Office for People With Developmental Disabilities · US

Funding

Abnormal Hyperphosphorylation of TauR01AG019158 · NIA · INSTITUTE FOR BASIC RES IN DEV DISABIL · PI IQBAL, KHALID · 2002 to 2011
$3.7M
I2PP2A: A Therapeutic TargetR03TW008744 · FIC · INSTITUTE FOR BASIC RES IN DEV DISABIL · PI IQBAL, KHALID · 2011 to 2013
$208k
FIC NIH HHS R03 TW008744FIC NIH HHS TW008744NIA NIH HHS AG019158NIA NIH HHS R01 AG019158
6 · The paper itself

Abstract

The bulk of AD research during the last 25 years has been Aβ-centric based on a strong faith in the Amyloid Cascade Hypothesis which is not supported by the data on humans. To date, Aβ-based therapeutic clinical trials on sporadic cases of AD have been negative. Although most likely the major reason for the failure is that Aβ is not an effective therapeutic target for sporadic AD, initiation of the treatment at mild to moderate stages of the disease is blamed as too late to be effective. Clinical trials on presymptomatic familial AD cases have been initiated with the logic that Aβ is a trigger of the disease and hence initiation of the Aβ immunotherapies several years before any clinical symptoms would be effective. There is an urgent need to explore targets other than Aβ. There is now increasing interest in inhibiting tau pathology, which does have a far more compelling rationale than Aβ. AD is multifactorial and over 99% of the cases are the sporadic form of the disease. Understanding of the various etiopathogenic mechanisms of sporadic AD and generation of the disease-relevant animal models are required to develop rational therapeutic targets and therapies. Treatment of AD will require both inhibition of neurodegeneration and regeneration of the brain.

Indexed as

Neurofibrillary TanglesPlaque, AmyloidAlzheimer DiseaseHumansImmunotherapyPhosphorylationtau Proteinstau ProteinsAbnormal hyperphosphorylation of tauAβNeurofibrillary tanglesNeuroregenerationPlaquesProtein phosphatase-2ATauopathies

Identifiers

PMID24418409
PMCPMC4024824
OpenAlexW2147606255

What OpenQuestion holds

Textmetadata
LicenceTDM
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.