Evidence map›Paper›PMID 39931856›Full record

ReviewCurrent Alzheimer research2024

Tauopathy in AD: Therapeutic Potential of MARK-4.

Mumtaz, Faraha Ahmed, Syed Arman Rabbani, Mohamed El-Tanani, Abul Kalam Najmi, Javed Ali, Mohammad Ahmed Khan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current Alzheimer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

7 authors.

MumtazDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India.
Faraha AhmedDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India.
Syed Arman RabbaniRAK College of Pharmacy, RAK Medical and Health Sciences University, Ras Al Khaimah, United Arab Emirates.
Mohamed El-TananiRAK College of Pharmacy, RAK Medical and Health Sciences University, Ras Al Khaimah, United Arab Emirates.
Abul Kalam NajmiDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India.
Javed AliDepartment of Pharmaceutics, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India.
Mohammad Ahmed KhanDepartment of Pharmacology, School of Pharmaceutical Education and Research, Jamia Hamdard, New Delhi, 110062, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is one of the leading causes of cognitive decline, which leads to dementia and poses significant challenges for its therapy. The reason is primarily the ineffective available treatments targeting the underlying pathology of AD. It is a neurodegenerative disease that is mainly characterised by the various molecular pathways contributing to its complex pathology, including extracellular amyloid beta (Aβ) plaques, intracellular neurofibrillary tangles (NFTs), oxidative stress, and neuroinflammation. One of the crucial features is the hyperphosphorylation of tau proteins, which is facilitated by microtubule affinity-regulating kinase-4 (MARK-4). The kinase plays a crucial role in the disease development by modifying microtubule integrity, leading to neuronal dysfunction and death. MARK-4 is thus a druggable target and has a pivotal role in AD. Amongst MARK-4 inhibitors, 16 compounds demonstrate significant capacity in molecular docking studies, showing high binding affinity to MARK-4 and promising potential for tau inhibition. Further,

Indexed as

Alzheimer DiseaseProtein Serine-Threonine KinasesTauopathiestau ProteinsAnimalsHumansNeuroprotective AgentsMARK4 protein, humanNeuroprotective AgentsProtein Serine-Threonine Kinasestau ProteinsAlzheimer’s diseasein silicoin vitroMARK-4neuronal dysfunction.oxidative stresstau proteins

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.