SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
American Journal of Alzheimer's Disease and Other Dementias®
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
1533317509346209v1
1533317509346209v2
24/6/456    most recent
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Gliebus, G.
Right arrow Articles by Lippa, C. F.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gliebus, G.
Right arrow Articles by Lippa, C. F.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Progranulin and β-Amyloid Distribution: A Case Report of the Brain From Preclinical PS-1 Mutation Carrier

Gediminas Gliebus, MD

Department of Neurology, Drexel University College of Medicine, Philadelphia, Pennsylvania

Andrea Rosso, MPH

Department of Neurology, Drexel University College of Medicine, Philadelphia, Pennsylvania

Carol F. Lippa, MD

Department of Neurology, Drexel University College of Medicine, Philadelphia, Pennsylvania, clippa{at}drexelmed.edu

Background: Progranulin (PGRN) is a multifunctional growth factor that is found in many tissues. Mutations in the PGRN gene cause familial frontotemporal dementia with ubiquitin-positive inclusions. PGRN plaque-like structures have been described in Alzheimer’s disease (AD), in association with β-amyloid (Aβ) plaques. Objective: To investigate PGRN and aggregated Aβ immunolabeling distribution in autopsied brain tissue from the participant with confirmed PS-1 (A246E) mutation, who died prior to clinical symptom onset. Results: Immunolabeling for PGRN was positive and accumulated/formed plaque-like structures in all studied regions. These structures most frequently colocalized with Aβ though there were some that did not. PGRN plaques were most dense in medial temporal and frontal regions and predominated over aggregated Aβ. Conclusions: This case report illustrates PGRN accumulation and Aβ aggregation in preclinical PS-1 AD case and raises the question whether this phenomenon coincides with or precedes Aβ aggregation.

Key Words: progranulin • Alzheimer’s disease • PS-1 mutation • β-amyloid

This version was published on December 1, 2009

American Journal of Alzheimer's Disease and Other Dementias®, Vol. 24, No. 6, 456-460 (2009)
DOI: 10.1177/1533317509346209


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?




Advertisement