Evidence map›Paper›PMID 37332018›Full record

ReviewMolecular neurobiology2023

Pathological Impact of Tau Proteolytical Process on Neuronal and Mitochondrial Function: a Crucial Role in Alzheimer's Disease.

Margrethe A Olesen, Rodrigo A Quintanilla

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Margrethe A OlesenLaboratory of Neurodegenerative Diseases, Facultad de Ciencias de La Salud, Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, El Llano Subercaseaux 2801, 5to Piso, San Miguel, 8910060, Santiago, Chile.
Rodrigo A QuintanillaLaboratory of Neurodegenerative Diseases, Facultad de Ciencias de La Salud, Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, El Llano Subercaseaux 2801, 5to Piso, San Miguel, 8910060, Santiago, Chile. rodrigo.quintanilla@uautonoma.cl.ORCID http://orcid.org/0000-0002-9582-6379
Universidad Autónoma de Chile · CL

Funding

ANID, FONDECYT 1200178
6 · The paper itself

Abstract

Tau protein plays a pivotal role in the central nervous system (CNS), participating in microtubule stability, axonal transport, and synaptic communication. Research interest has focused on studying the role of post-translational tau modifications in mitochondrial failure, oxidative damage, and synaptic impairment in Alzheimer's disease (AD). Soluble tau forms produced by its pathological cleaved induced by caspases could lead to neuronal injury contributing to oxidative damage and cognitive decline in AD. For example, the presence of tau cleaved by caspase-3 has been suggested as a relevant factor in AD and is considered a previous event before neurofibrillary tangles (NFTs) formation.Interestingly, we and others have shown that caspase-cleaved tau in N- or C- terminal sites induce mitochondrial bioenergetics defects, axonal transport impairment, neuronal injury, and cognitive decline in neuronal cells and murine models. All these abnormalities are considered relevant in the early neurodegenerative manifestations such as memory and cognitive failure reported in AD. Therefore, in this review, we will discuss for the first time the importance of truncated tau by caspases activation in the pathogenesis of AD and how its negative actions could impact neuronal function.

Indexed as

Alzheimer DiseaseAnimalsCaspasesHumansMiceMitochondriaNeuronstau ProteinsCaspasestau ProteinsAlzheimer’s diseaseCaspaseMitochondriaNeurodegenerationSynaptic lossTau

Identifiers

PMID37332018
OpenAlexW4381122766

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.