Evidence map›Paper›PMID 29572646›Full record

ArticleNeurochemical research2019

Knockout of Amyloid β Protein Precursor (APP) Expression Alters Synaptogenesis, Neurite Branching and Axonal Morphology of Hippocampal Neurons.

Katherine A Southam, Fiona Stennard, Cassandra Pavez, David H Small

Abstract read
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In one paragraph

Article in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Kat5 cKO mouse replicates biological domain signatures associated with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Synaptogenic effect ofScience translational medicine · 2022
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. 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

4 authors at 1 institution in 1 country.

Katherine A SouthamMenzies Institute for Medical Research, University of Tasmania, Hobart, TAS, 7000, Australia. Katherine.Southam@utas.edu.au.ORCID http://orcid.org/0000-0003-3171-6928
Fiona StennardMenzies Institute for Medical Research, University of Tasmania, Hobart, TAS, 7000, Australia.
Cassandra PavezMenzies Institute for Medical Research, University of Tasmania, Hobart, TAS, 7000, Australia.
David H SmallMenzies Institute for Medical Research, University of Tasmania, Hobart, TAS, 7000, Australia.
University of Tasmania · AU

Funding

Alzheimer's Australia Dementia Research Foundation S0022366National Health and Medical Research Council APP1042566University of Tasmania S0022901
6 · The paper itself

Abstract

The function of the β-A4 amyloid protein precursor (APP) of Alzheimer's disease (AD) remains unclear. APP has a number of putative roles in neuronal differentiation, survival, synaptogenesis and cell adhesion. In this study, we examined the development of axons, dendrites and synapses in cultures of hippocampus neutrons derived from APP knockout (KO) mice. We report that loss of APP function reduces the branching of cultured hippocampal neurons, resulting in reduced synapse formation. Using a compartmentalised culture approach, we found reduced axonal outgrowth in cultured hippocampal neurons and we also identified abnormal growth characteristics of isolated hippocampal neuron axons. Although APP has previously been suggested to play an important role in promoting cell adhesion, we surprisingly found that APPKO hippocampal neurons adhered more strongly to a poly-L-lysine substrate and their neurites displayed an increased density of focal adhesion puncta. The findings suggest that the function of APP has an important role in both dendritic and axonal growth and that endogenous APP may regulate substrate adhesion of hippocampal neurons. The results may explain neuronal and synaptic morphological abnormalities in APPKO mice and the presence of abnormal APP expression in dystrophic neurites around amyloid deposits in AD.

Indexed as

Amyloid beta-Protein PrecursorAnimalsAxonsCell AdhesionDendritesFemaleGene Knockout TechniquesHippocampusMice, Inbred C57BLMice, KnockoutNeuronal OutgrowthPregnancySynapsesAmyloid beta-Protein PrecursorAlzheimer’s diseaseAmyloidAPPAxon pathfindingNeurite outgrowth

Identifiers

PMID29572646
OpenAlexW2793954600

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.