Evidence map›Paper›PMID 26351077›Full record

SynthesisMolecular neurobiology2016

Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.

Puneet Talwar, Juhi Sinha, Sandeep Grover, Chitra Rawat, Suman Kushwaha, Rachna Agarwal, Vibha Taneja, Ritushree Kukreti

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
–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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  6. Review
  7. Review
  8. Unveiling the Therapeutic Potential ofBioMed research international · 2025
    Article
  9. Magnolol acts as a neurorestorative agent in an AExperimental and therapeutic medicine · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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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

8 authors.

Puneet TalwarAcademy of Scientific and Innovative Research (AcSIR), CSIR-Institute of Genomics and Integrative Biology (CSIR-IGIB) Campus, New Delhi, India.
Juhi SinhaGenomics and Molecular Medicine Unit, CSIR-Institute of Genomics and Integrative Biology (CSIR-IGIB), Mall Road, Delhi, 110 007, India.
Sandeep GroverGenomics and Molecular Medicine Unit, CSIR-Institute of Genomics and Integrative Biology (CSIR-IGIB), Mall Road, Delhi, 110 007, India.
Chitra RawatAcademy of Scientific and Innovative Research (AcSIR), CSIR-Institute of Genomics and Integrative Biology (CSIR-IGIB) Campus, New Delhi, India.
Suman KushwahaInstitute of Human Behaviour and Allied Sciences (IHBAS), Delhi, India.
Rachna AgarwalInstitute of Human Behaviour and Allied Sciences (IHBAS), Delhi, India.
Vibha TanejaDepartment of Research, Sir Ganga Ram Hospital, New Delhi, India.
Ritushree KukretiAcademy of Scientific and Innovative Research (AcSIR), CSIR-Institute of Genomics and Integrative Biology (CSIR-IGIB) Campus, New Delhi, India. ritus@igib.res.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by loss of memory and other cognitive functions. AD can be classified into familial AD (FAD) and sporadic AD (SAD) based on heritability and into early onset AD (EOAD) and late onset AD (LOAD) based on age of onset. LOAD cases are more prevalent with genetically complex architecture. In spite of significant research focused on understanding the etiological mechanisms, search for diagnostic biomarker(s) and disease-modifying therapy is still on. In this article, we aim to comprehensively review AD literature on established etiological mechanisms including role of beta-amyloid and apolipoprotein E (APOE) along with promising newer etiological factors such as epigenetic modifications that have been associated with AD suggesting its multifactorial nature. As genomic studies have recently played a significant role in elucidating AD pathophysiology, a systematic review of findings from genome-wide linkage (GWL), genome-wide association (GWA), genome-wide expression (GWE), and epigenome-wide association studies (EWAS) was conducted. The availability of multi-dimensional genomic data has further coincided with the advent of computational and network biology approaches in recent years. Our review highlights the importance of integrative approaches involving genomics and systems biology perspective in elucidating AD pathophysiology. The promising newer approaches may provide reliable means of early and more specific diagnosis and help identify therapeutic interventions for LOAD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoproteins EEpigenomicsGenetic Predisposition to DiseaseGenome-Wide Association StudyGenomicsHumansSystems BiologyAmyloid beta-PeptidesApolipoproteins EAlzheimer’s diseaseEndophenotypeEpigeneticsEtiologyGenome-wide associationGenome-wide expression studiesGenome-wide linkage

Identifiers

What OpenQuestion holds

Textmetadata
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.