Evidence map›Paper›PMID 35011577›Full record

ReviewCells2021

The Nerve Growth Factor Metabolic Pathway Dysregulation as Cause of Alzheimer's Cholinergic Atrophy.

Sonia Do Carmo, Benjamin Kannel, A Claudio Cuello

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
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  14. NGF and Its Role in Immunoendocrine Communication during Metabolic Syndrome.International journal of molecular sciences · 2023
    Review
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  16. Review
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

3 authors.

Sonia Do CarmoDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC H3G 1Y6, Canada.
Benjamin KannelDepartment of Neurology and Neurosurgery, McGill University, Montreal, QC H3A 2B4, Canada.
A Claudio CuelloDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC H3G 1Y6, Canada.

Funding

CIHR 201603PJT-364544National Institute of Health and Aging R01 AG056850
6 · The paper itself

Abstract

The cause of the loss of basal forebrain cholinergic neurons (BFCNs) and their terminal synapses in the cerebral cortex and hippocampus in Alzheimer's disease (AD) has provoked a decades-long controversy. The cholinergic phenotype of this neuronal system, involved in numerous cognitive mechanisms, is tightly dependent on the target-derived nerve growth factor (NGF). Consequently, the loss of BFCNs cholinergic phenotype in AD was initially suspected to be due to an NGF trophic failure. However, in AD there is a normal NGF synthesis and abundance of the NGF precursor (proNGF), therefore the NGF trophic failure hypothesis for the atrophy of BCNs was abandoned. In this review, we discuss the history of NGF-dependency of BFCNs and the atrophy of these neurons in Alzheimer's disease (AD). Further to it, we propose that trophic factor failure explains the BFCNs atrophy in AD. We discuss evidence of the occurrence of a brain NGF metabolic pathway, the dysregulation of which, in AD explains the severe deficiency of NGF trophic support for the maintenance of BFCNs cholinergic phenotype. Finally, we revise recent evidence that the NGF metabolic dysregulation in AD pathology starts at preclinical stages. We also propose that the alteration of NGF metabolism-related markers in body fluids might assist in the AD preclinical diagnosis.

Indexed as

Metabolic Networks and PathwaysAlzheimer DiseaseAnimalsAtrophyCholinergic NeuronsHumansNerve Growth FactorSynapsesNerve Growth FactorAlzheimer’s diseasebasal forebrain cholinergic nucleicholinergic systemDown syndromenerve growth factorNGF metabolic cascadetrophic support

Identifiers

PMID35011577
PMCPMC8750266

What OpenQuestion holds

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Registered trials

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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.