Evidence map›Paper›PMID 32765949›Full record

ReviewAging and disease2020

TGF-β Signaling: A Therapeutic Target to Reinstate Regenerative Plasticity in Vascular Dementia?

Mahesh Kandasamy, Muthuswamy Anusuyadevi, Kiera M Aigner, Michael S Unger, Kathrin M Kniewallner, Diana M Bessa de Sousa, Barbara Altendorfer, Heike Mrowetz, Ulrich Bogdahn, Ludwig Aigner

Open access · goldAbstract readReview
In one paragraph

Review in Aging and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 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

10 authors at 3 institutions in 3 countries.

Mahesh Kandasamy1Laboratory of Stem Cells and Neuroregeneration, Department of Animal Science, School of Life Sciences, Bharathidasan University, Tiruchirappalli, Tamil Nadu, India.
Muthuswamy Anusuyadevi3Molecular Gerontology Group, Department of Biochemistry, School of Life Sciences, Bharathidhasan University, Tiruchirappalli, Tamil Nadu, India.
Kiera M Aigner4Institute of Molecular Regenerative Medicine, Salzburg, Paracelsus Medical University.
Michael S Unger4Institute of Molecular Regenerative Medicine, Salzburg, Paracelsus Medical University.
Kathrin M Kniewallner4Institute of Molecular Regenerative Medicine, Salzburg, Paracelsus Medical University.
Diana M Bessa de Sousa4Institute of Molecular Regenerative Medicine, Salzburg, Paracelsus Medical University.
Barbara Altendorfer4Institute of Molecular Regenerative Medicine, Salzburg, Paracelsus Medical University.
Heike Mrowetz4Institute of Molecular Regenerative Medicine, Salzburg, Paracelsus Medical University.
Ulrich Bogdahn4Institute of Molecular Regenerative Medicine, Salzburg, Paracelsus Medical University.
Ludwig Aigner4Institute of Molecular Regenerative Medicine, Salzburg, Paracelsus Medical University.
Paracelsus Medical University · ATBharathidasan University · INUniversity Grants Commission · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular dementia (VaD) is the second leading form of memory loss after Alzheimer's disease (AD). Currently, there is no cure available. The etiology, pathophysiology and clinical manifestations of VaD are extremely heterogeneous, but the impaired cerebral blood flow (CBF) represents a common denominator of VaD. The latter might be the result of atherosclerosis, amyloid angiopathy, microbleeding and micro-strokes, together causing blood-brain barrier (BBB) dysfunction and vessel leakage, collectively originating from the consequence of hypertension, one of the main risk factors for VaD. At the histopathological level, VaD displays abnormal vascular remodeling, endothelial cell death, string vessel formation, pericyte responses, fibrosis, astrogliosis, sclerosis, microglia activation, neuroinflammation, demyelination, white matter lesions, deprivation of synapses and neuronal loss. The transforming growth factor (TGF) β has been identified as one of the key molecular factors involved in the aforementioned various pathological aspects. Thus, targeting TGF-β signaling in the brain might be a promising therapeutic strategy to mitigate vascular pathology and improve cognitive functions in patients with VaD. This review revisits the recent understanding of the role of TGF-β in VaD and associated pathological hallmarks. It further explores the potential to modulate certain aspects of VaD pathology by targeting TGF-β signaling.

Indexed as

BBBendothelial cellshippocampusneural regenerationoxidative stresspericytesTGF-βvascular dementia

Identifiers

PMID32765949
PMCPMC7390515
OpenAlexW3046693269

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.