Evidence map›Paper›PMID 9185547›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997

Neuronal localization of presenilin-1 and association with amyloid plaques and neurofibrillary tangles in Alzheimer's disease.

J Busciglio, H Hartmann, A Lorenzo, C Wong, K Baumann, B Sommer, M Staufenbiel, B A Yankner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Differential release of β-amyloid from dendrite- versus axon-targeted APP.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  5. Early onset Alzheimer's disease and oxidative stress.Oxidative medicine and cellular longevity · 2014
    Review
  6. CSF Presenilin-1 complexes are increased in Alzheimer's disease.Acta neuropathologica communications · 2013
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Presenilin 1 forms aggresomal deposits in response to heat shock.Journal of molecular neuroscience : MN · 2006
    Article
  14. Article
  15. Article
  16. Alzheimer's presenilin 1 mutations impair kinesin-based axonal transport.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  17. Aberrant activation of focal adhesion proteins mediates fibrillar amyloid beta-induced neuronal dystrophy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  18. Article
  19. Article
  20. Article
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

8 authors at 2 institutions in 1 country.

J BusciglioDepartment of Neurology, Harvard Medical School and Division of Neuroscience, The Children's Hospital, Boston, Massachusetts 02115, USA.
H Hartmann
A Lorenzo
C Wong
K Baumann
B Sommer
M Staufenbiel
B A Yankner
Harvard University · USBoston Children's Hospital · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Studies on the Mechanism of Beta Amyloid NeurotoxicityR01NS030352 · NINDS · HARVARD MEDICAL SCHOOL · PI YANKNER, BRUCE A · 1992 to 2007
$2.3M
MECHANISMS OF NEURONAL DEGENERATION IN DOWNS SYNDROMER01NS033325 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI YANKNER, BRUCE A · 1996 to 1998
–
NICHD NIH HHS P30 HD018655NICHD NIH HHS P30-HD18655NINDS NIH HHS NS30352NINDS NIH HHS NS33325NINDS NIH HHS R01 NS030352
6 · The paper itself

Abstract

Mutations in the presenilin-1 (PS1) gene is a cause of early- onset familial Alzheimer's disease (AD). Endogenous PS1 is associated with the endoplasmic reticulum in the cell body of undifferentiated SH-SY5Y neuroblastoma cells. At early stages of neuronal differentiation in rat hippocampal culture, PS1 appears in all neuritic processes and in growth cones. In mature differentiated neurons, PS1 is concentrated in the somatodendritic compartment but is also present at lower levels in axons. A similar localization of PS1 is observed in vivo in neurons of the adult human cerebral cortex. In sporadic AD, PS1 appears in the dystrophic neurites of mature amyloid plaques and co-localizes with a subset of intraneuronal neurofibrillary tangles (NFTs). About 30% of hippocampal NFTs are labeled with a highly specific antibody to the PS1 C-terminal loop domain but not with an antibody to the PS1 N terminus. This observation is consistent with a potential association of the PS1 C-terminal fragment with NFTs, because PS1 is constitutively cleaved to N- and C-terminal fragments in neurons. These results suggest that PS1 is highly expressed and broadly distributed during early stages of neuronal differentiation, consistent with a role for PS1 in neuronal differentiation. Furthermore, the co-localization of PS1 with NFTs and plaque dystrophic neurites implicates a role for PS1 in the diverse pathological manifestations of AD.

Indexed as

Alzheimer DiseaseAmyloidAnimalsBrainCell DifferentiationHumansMembrane ProteinsNeuritesNeurofibrillary TanglesNeuronsPresenilin-1RatsTissue DistributionTransfectionAmyloidMembrane ProteinsPresenilin-1PSEN1 protein, human

Identifiers

PMID9185547
PMCPMC6573321
OpenAlexW1952363942

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.