Evidence map›Paper›PMID 22327870›Full record

ArticleNeuro-degenerative diseases2012

Evaluation of neurodegeneration in a mouse model of infantile batten disease by magnetic resonance imaging and magnetic resonance spectroscopy.

Jeeva Munasinghe, Zhongjian Zhang, Eryan Kong, Alison Heffer, Anil B Mukherjee

Open access · bronzeAbstract readEvaluation Study
In one paragraph

Article in Neuro-degenerative diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Article
  3. GFAP hyperpalmitoylation exacerbates astrogliosis and neurodegenerative pathology in PPT1-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  4. Article
  5. Article
  6. 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

5 authors at 3 institutions in 1 country.

Jeeva MunasingheIn Vivo NMR Center-HNQ2-3, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1830, USA. mukherja@exchange.nih.gov
Zhongjian Zhang
Eryan Kong
Alison Heffer
Anil B Mukherjee
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institute of Neurological Disorders and Stroke · US

Funding

Neurodegenerative Lysosomal Storage DisordersZIAHD000910 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MUKHERJEE, ANIL B · 2009 to 2025
$24.1M
Intramural NIH HHS
6 · The paper itself

Abstract

Neuronal ceroid lipofuscinoses (NCLs) represent a group of common hereditary childhood neurodegenerative storage disorders that have no effective treatment. Mutations in eight different genes cause various forms of NCLs. Infantile NCL (INCL), the most lethal disease, is caused by inactivating mutations in the palmitoyl-protein thioesterase-1 (PPT1) gene. The availability of Ppt1-knockout (Ppt1-KO) mice, which recapitulate virtually all clinical and pathological features of INCL, provides an opportunity to test the effectiveness of novel therapeutic strategies in vivo. However, such studies will require noninvasive methods that can be used to perform serial evaluations of the same animal receiving an experimental therapy. Thus, the development of noninvasive method(s) of evaluation is urgently needed. Here, we report our evaluation of the progression of neurodegeneration in Ppt1-KO mice starting at 3 months of age by MRI and MR spectroscopy (MRS) and repeating these tests using the same mice at 4, 5 and 6 months of age. Our results showed progressive cerebral atrophy, which was associated with histological loss of neuronal content and increase in astroglia. Remarkably, while the brain volumes in Ppt1-KO mice progressively declined with advancing age, the MRS signals, which were significantly lower than those of their wild-type littermates, remained virtually unchanged from 3 to 6 months of age. In addition, our results also showed an abnormality in cerebral blood flow in these mice, which showed progression with age. Our findings provide methods to serially examine the brains of mouse models of neurodegenerative diseases (e.g. Ppt1-KO mice) using noninvasive and nonlethal procedures such as MRI and MRS. These methods may be useful in studies to understand the progression of neuropathology in animal models of neurodegenerative diseases as they allow repeated evaluations of the same animal in which experimental therapies are tested.

Indexed as

Disease ProgressionAgingAnimalsAstrocytesBrainDisease Models, AnimalFemaleMagnetic Resonance ImagingMagnetic Resonance SpectroscopyMaleMiceMice, Inbred C57BLMice, KnockoutNeurodegenerative DiseasesNeuronal Ceroid-LipofuscinosesNeuronspalmitoyl-protein thioesteraseThiolester Hydrolases

Identifiers

PMID22327870
PMCPMC3369263
OpenAlexW1987709807

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.