Evidence map›Paper›PMID 42443606›Full record

ReviewInflammopharmacology2026

Tau physiology and pathology: impacts on cellular structures and neurodegenerative diseases.

Vali Akbari, Seifollah Bahramikia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Vali AkbariDepartment of Biology, Faculty of Basic Sciences, Lorestan University, Khorramabad, Iran. akbari.v@lu.ac.ir.
Seifollah BahramikiaDepartment of Biology, Faculty of Basic Sciences, Lorestan University, Khorramabad, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review explores the crucial roles of the tau protein in neuronal integrity and its dysregulation in neurodegenerative diseases (NDs), particularly tauopathies. Key features include abnormal tau phosphorylation, leading to insoluble aggregates and neuronal dysfunction. Various therapeutic strategies, such as reducing tau phosphorylation, inhibiting aggregation, and enhancing clearance through autophagy and immunotherapies, are discussed. Promising candidates such as anle138b and methylene blue display efficacy in preclinical models. The interplay between tau and Aβ pathology is also highlighted, emphasizing the complexity of therapeutic approaches. A thorough understanding of tau functions is essential for developing targeted treatments to combat tau-related neurotoxicity and advance therapies for Alzheimer's disease (AD). This article examines the dual role of tau in physiology and pathology, highlighting its effects at both the cellular and subcellular levels. These findings underscore the critical importance of the tau protein in preventing NDs and suggest that a deeper understanding of its functions could improve treatment strategies for tau-related disorders.

Indexed as

Neurodegenerative DiseasesTauopathiestau ProteinsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsHumansNeuronsPhosphorylationAmyloid beta-Peptidestau ProteinsAggregationAlzheimer's diseaseNeurodegenerative diseasesTauopathies

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.