Evidence map›Paper›PMID 31209782›Full record

ReviewMolecular neurobiology2019

Melatonin in Alzheimer's Disease: A Latent Endogenous Regulator of Neurogenesis to Mitigate Alzheimer's Neuropathology.

Md Farhad Hossain, Md Sahab Uddin, G M Sala Uddin, Dewan Md Sumsuzzman, Md Siddiqul Islam, George E Barreto, Bijo Mathew, Ghulam Md Ashraf

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
9.0field-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.

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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 133 citations in OpenAlex.

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  19. Exploring the role of COX-2 in Alzheimer's disease: Potential therapeutic implications of COX-2 inhibitors.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
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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 at 6 institutions in 6 countries.

Md Farhad HossainDepartment of Physical Therapy, Graduate School of Inje University, Gimhae, South Korea.
Md Sahab UddinDepartment of Pharmacy, Southeast University, Dhaka, Bangladesh. msu-neuropharma@hotmail.com.ORCID http://orcid.org/0000-0002-0805-7840
G M Sala UddinDepartment of Pharmacy, Southeast University, Dhaka, Bangladesh.
Dewan Md SumsuzzmanDepartment of Rehabilitation Science, Graduate School of Inje University, Gimhae, South Korea.
Md Siddiqul IslamDepartment of Pharmacy, Southeast University, Dhaka, Bangladesh.
George E BarretoDepartamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá DC, Colombia.
Bijo MathewDivision of Drug Design and Medicinal Chemistry Research Lab, Department of Pharmaceutical Chemistry, Ahalia School of Pharmacy, Palakkad, India.
Ghulam Md AshrafKing Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia. ashraf.gm@gmail.com.ORCID http://orcid.org/0000-0002-9820-2078
Inje University · KRSoutheast University · BDKerala School of Mathematics · INKing Abdulaziz University · SAPontificia Universidad Javeriana · COUttara University · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melatonin, a pineal gland synthesized neurohormone is known as a multifunctioning pleiotropic agent which has a wide range of neuroprotective role in manifold age-related neurodegenerative disorders especially Alzheimer's diseases (AD). AD is a devastating neurodegenerative disorder and common form of dementia which is defined by abnormal and excessive accumulation of several toxic peptides including amyloid β (Aβ) plaques and neurofibrillary tangles (NFTs). The Alzheimer's dementia relates to atrophic changes in the brain resulting in loss of memory, cognitive dysfunction, and impairments of the synapses. Aging, circadian disruption, Aβ accumulation, and tau hyperphosphorylation are the utmost risk factor regarding AD pathology. To date, there is no exact treatment against AD progression. In this regard, melatonin plays a crucial role for the inhibition of circadian disruption by controlling clock genes and also attenuates Aβ accumulation and tau hyperphosphorylation by regulating glycogen synthase kinase-3 (GSK3) and cyclin-dependent kinase-5 (CDK5) signaling pathway. In this review, we highlight the possible mechanism of AD etiology and how melatonin influences neurogenesis by attenuating circadian disruption, Aβ formation, as well as tau hyperphosphorylation. Furthermore, we also find out and summarize the neuroprotective roles of melatonin by the blockage of Aβ production, Aβ oligomerization and fibrillation, tau hyperphosphorylation, synaptic dysfunction, oxidative stress, and neuronal death during AD progression.

Indexed as

NeurogenesisAlzheimer DiseaseAnimalsBrainCircadian RhythmHumansMelatoninMolecular Targeted TherapyMelatoninAlzheimer’s diseaseAmyloid βCircadian rhythmMelatoninNeurofibrillary tangles

Identifiers

PMID31209782
OpenAlexW2951065316

What Socratic 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 Socratic graph.