Evidence map›Paper›PMID 28266222›Full record

ArticleASN neuro

Conditional Depletion of Hippocampal Brain-Derived Neurotrophic Factor Exacerbates Neuropathology in a Mouse Model of Alzheimer's Disease.

David J Braun, Sergey Kalinin, Douglas L Feinstein

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Noradrenaline in Alzheimer's Disease: A New Potential Therapeutic Target.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. p75Glia · 2019
    Article
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  16. Article
  17. Review
  18. Article
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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 2 institutions in 1 country.

David J Braun1 Department of Anesthesiology, University of Illinois, Chicago, IL, USA.
Sergey Kalinin1 Department of Anesthesiology, University of Illinois, Chicago, IL, USA.
Douglas L Feinstein2 Jesse Brown VA Medical Center, Chicago, IL, USA.
University of Illinois Chicago · USJesse Brown VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Damage occurring to noradrenergic neurons in the locus coeruleus (LC) contributes to the evolution of neuroinflammation and neurodegeneration in a variety of conditions and diseases. One cause of LC damage may be loss of neurotrophic support from LC target regions. We tested this hypothesis by conditional unilateral knockout of brain-derived neurotrophic factor (BDNF) in adult mice. To evaluate the consequences of BDNF loss in the context of neurodegeneration, the mice harbored familial mutations for human amyloid precursor protein and presenilin-1. In these mice, BDNF depletion reduced tyrosine hydroxylase staining, a marker of noradrenergic neurons, in the rostral LC. BDNF depletion also reduced noradrenergic innervation in the hippocampus, the frontal cortex, and molecular layer of the cerebellum, assessed by staining for dopamine beta hydroxylase. BDNF depletion led to an increase in cortical amyloid plaque numbers and size but was without effect on plaque numbers in the striatum, a site with minimal innervation from the LC. Interestingly, cortical Iba1 staining for microglia was reduced by BDNF depletion and was correlated with reduced dopamine beta hydroxylase staining. These data demonstrate that reduction of BDNF levels in an LC target region can cause retrograde damage to LC neurons, leading to exacerbation of neuropathology in distinct LC target areas. Methods to reduce BDNF loss or supplement BDNF levels may be of value to reduce neurodegenerative processes normally limited by LC noradrenergic activities.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBrain-Derived Neurotrophic FactorCalcium-Binding ProteinsDisease Models, AnimalHippocampusHumansLocus CoeruleusMice, 129 StrainMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsMicrogliaNeuronsPlaque, AmyloidAif1 protein, mouseAmyloid beta-Protein PrecursorAPP protein, humanBrain-Derived Neurotrophic FactorCalcium-Binding ProteinsMicrofilament ProteinsPresenilin-1PSEN1 protein, humanadeno-associated virusAlzheimer’s diseaseamyloidbrain-derived neurotrophic factorlocus coeruleusneuroinflammationneurotrophinnoradrenalinetyrosine hydroxylase

Identifiers

PMID28266222
PMCPMC5415058
OpenAlexW2593244758

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.