Evidence map›Paper›PMID 32052374›Full record

ReviewCNS drugs2020

Born to Protect: Leveraging BDNF Against Cognitive Deficit in Alzheimer's Disease.

Lucia Caffino, Francesca Mottarlini, Fabio Fumagalli

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in CNS drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. Simvastatin rescues cognitive impairment in an AβNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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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

3 authors at 1 institution in 1 country.

Lucia CaffinoDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Via Balzaretti 9, 20133, Milan, Italy.
Francesca MottarliniDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Via Balzaretti 9, 20133, Milan, Italy.
Fabio FumagalliDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Via Balzaretti 9, 20133, Milan, Italy. Fabio.Fumagalli@unimi.it.ORCID 0000-0002-8814-7706
University of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is a chronic neurodegenerative devastating disorder affecting a high percentage of the population over 65 years of age and causing a relevant emotional, social, and economic burden. Clinically, it is characterized by a prominent cognitive deficit associated with language and behavioral impairments. The molecular pathogenesis of Alzheimer's disease is multifaceted and involves changes in neurotransmitter levels together with alterations of inflammatory, oxidative, hormonal, and synaptic pathways, which may represent a drug target for both prevention and treatment; however, an effective treatment for Alzheimer's disease still represents an unmet goal. As neurotrophic factors participate in the modulation of the above-mentioned pathways, they have been highlighted as critical contributors of Alzheimer's disease etiology, whose modulation might be beneficial for Alzheimer's disease. We focused on the neurotrophin brain-derived neurotrophic factor, providing several lines of evidence pointing to brain-derived neurotrophic factor as a plausible endophenotype of cognitive deficits in Alzheimer's disease, illustrating some of the most recent possibilities to modulate the expression of this neurotrophin in the brain in an attempt to ameliorate cognition and delay the progression of Alzheimer's disease. This review shows that otherwise disparate pharmacologic or non-pharmacologic approaches converge on brain-derived neurotrophic factor, providing a means whereby apparently unrelated medical approaches may nevertheless produce similar synaptic and cognitive outcomes in Alzheimer's disease pathogenesis, suggesting that brain-derived neurotrophic factor-based synaptic repair may represent a modifying strategy to ameliorate cognition in Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsBrainBrain-Derived Neurotrophic FactorCognitionCognition DisordersHumansNeuronsBrain-Derived Neurotrophic Factor

Identifiers

PMID32052374
OpenAlexW3006430273

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.