Evidence map›Paper›PMID 29441009›Full record

ReviewFrontiers in aging neuroscience2018

Autophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implications.

Md Sahab Uddin, Anna Stachowiak, Abdullah Al Mamun, Nikolay T Tzvetkov, Shinya Takeda, Atanas G Atanasov, Leandro B Bergantin, Mohamed M Abdel-Daim, Adrian M Stankiewicz

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04729855 (Association of Autophagy-related Genes ,LncRNA and SNPs With Colorectal Cancer in Egyptian Population), which is not on this map. Cited by 238 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed, 2 pooled it
32.1field-weighted citation impact, top 1% 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.

NCT04729855 completednot on this mapstarted 2022, after this paper: background citation

Association of Autophagy-related Genes ,LncRNA and SNPs With Colorectal Cancer in Egyptian Population

TypeobservationalSponsorEsraa Hassan,MDRan2022 to 2024Enrolled60ConditionsColo-rectal CancerArmsPBMCs and Tissue expression of HOTTIP ,EIF4EBP1 and serum SNP HOTTIP rs1859168
3 · Its place in the literature

Who cites it

238 citing papers in PubMed, 2 syntheses or guidelines pooled it, 450 citations in OpenAlex.

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178 more citing papers are in PubMed but not listed here.

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

9 authors at 7 institutions in 7 countries.

Md Sahab UddinDepartment of Pharmacy, Southeast University, Dhaka, Bangladesh.
Anna StachowiakDepartment of Experimental Embryology, Institute of Genetics and Animal Breeding, Polish Academy of Sciences, Magdalenka, Poland.
Abdullah Al MamunDepartment of Pharmacy, Southeast University, Dhaka, Bangladesh.
Nikolay T TzvetkovDepartment of Molecular Biology and Biochemical Pharmacology, Institute of Molecular Biology "Roumen Tsanev", Bulgarian Academy of Sciences, Sofia, Bulgaria.
Shinya TakedaDepartment of Clinical Psychology, Tottori University Graduate School of Medical Sciences, Tottori, Japan.
Atanas G AtanasovDepartment of Molecular Biology, Institute of Genetics and Animal Breeding, Polish Academy of Sciences, Magdalenka, Poland.
Leandro B BergantinDepartment of Pharmacology, Federal University of São Paulo, São Paulo, Brazil.
Mohamed M Abdel-DaimDepartment of Pharmacology, Suez Canal University, Ismailia, Egypt.
Adrian M StankiewiczDepartment of Molecular Biology, Institute of Genetics and Animal Breeding, Polish Academy of Sciences, Magdalenka, Poland.
Polish Academy of Sciences · PLSoutheast University · BDBulgarian Academy of Sciences · BGTottori University · JPUniversidade Federal de São Paulo · BRUniversity of Vienna · ATYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of progressive dementia in the elderly. It is characterized by a progressive and irreversible loss of cognitive abilities and formation of senile plaques, composed mainly of amyloid β (Aβ), and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus and cortex of afflicted humans. In brains of AD patients the metabolism of Aβ is dysregulated, which leads to the accumulation and aggregation of Aβ. Metabolism of Aβ and tau proteins is crucially influenced by autophagy. Autophagy is a lysosome-dependent, homeostatic process, in which organelles and proteins are degraded and recycled into energy. Thus, dysfunction of autophagy is suggested to lead to the accretion of noxious proteins in the AD brain. In the present review, we describe the process of autophagy and its importance in AD. Additionally, we discuss mechanisms and genes linking autophagy and AD, i.e., the mTOR pathway, neuroinflammation, endocannabinoid system,

Indexed as

Alzheimer’s diseaseamyloid betaautophagytau

Identifiers

PMID29441009
PMCPMC5797541
OpenAlexW2790720306

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.