No more brain tangles with ΔNp73

Mark P. Mattson; Uri Ashery

doi:10.1016/j.tibs.2008.10.004

No more brain tangles with ΔNp73

Mark P. Mattson, Uri Ashery

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

In Alzheimer's disease (AD), neurons suffer dysfunction and death associated with aberrant tau phosphorylation and subsequent neurofibrillary tangles. A new study reveals a surprising neuroprotective role for a truncated p73 isoform (ΔNp73). Aged mice with reduced ΔNp73 levels exhibit tau pathology and cognitive deficits, and ΔNp73 reduction in mice with amyloid pathology causes extensive tangle formation and neuron death. These findings provide a novel animal model of AD and a potential therapeutic role for ΔNp73 inducers.

Original language	English (US)
Pages (from-to)	6-8
Number of pages	3
Journal	Trends in Biochemical Sciences
Volume	34
Issue number	1
DOIs	https://doi.org/10.1016/j.tibs.2008.10.004
State	Published - Jan 2009
Externally published	Yes

ASJC Scopus subject areas

Biochemistry
Molecular Biology

Access to Document

10.1016/j.tibs.2008.10.004

Cite this

@article{007ad83f65f94b19a41823adbcad78e9,

title = "No more brain tangles with ΔNp73",

abstract = "In Alzheimer's disease (AD), neurons suffer dysfunction and death associated with aberrant tau phosphorylation and subsequent neurofibrillary tangles. A new study reveals a surprising neuroprotective role for a truncated p73 isoform (ΔNp73). Aged mice with reduced ΔNp73 levels exhibit tau pathology and cognitive deficits, and ΔNp73 reduction in mice with amyloid pathology causes extensive tangle formation and neuron death. These findings provide a novel animal model of AD and a potential therapeutic role for ΔNp73 inducers.",

author = "Mattson, {Mark P.} and Uri Ashery",

year = "2009",

month = jan,

doi = "10.1016/j.tibs.2008.10.004",

language = "English (US)",

volume = "34",

pages = "6--8",

journal = "Trends in Biochemical Sciences",

issn = "0968-0004",

publisher = "Elsevier Limited",

number = "1",

}

TY - JOUR

T1 - No more brain tangles with ΔNp73

AU - Mattson, Mark P.

AU - Ashery, Uri

PY - 2009/1

Y1 - 2009/1

N2 - In Alzheimer's disease (AD), neurons suffer dysfunction and death associated with aberrant tau phosphorylation and subsequent neurofibrillary tangles. A new study reveals a surprising neuroprotective role for a truncated p73 isoform (ΔNp73). Aged mice with reduced ΔNp73 levels exhibit tau pathology and cognitive deficits, and ΔNp73 reduction in mice with amyloid pathology causes extensive tangle formation and neuron death. These findings provide a novel animal model of AD and a potential therapeutic role for ΔNp73 inducers.

AB - In Alzheimer's disease (AD), neurons suffer dysfunction and death associated with aberrant tau phosphorylation and subsequent neurofibrillary tangles. A new study reveals a surprising neuroprotective role for a truncated p73 isoform (ΔNp73). Aged mice with reduced ΔNp73 levels exhibit tau pathology and cognitive deficits, and ΔNp73 reduction in mice with amyloid pathology causes extensive tangle formation and neuron death. These findings provide a novel animal model of AD and a potential therapeutic role for ΔNp73 inducers.

UR - http://www.scopus.com/inward/record.url?scp=58149178664&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=58149178664&partnerID=8YFLogxK

U2 - 10.1016/j.tibs.2008.10.004

DO - 10.1016/j.tibs.2008.10.004

M3 - Article

C2 - 19008105

AN - SCOPUS:58149178664

SN - 0968-0004

VL - 34

SP - 6

EP - 8

JO - Trends in Biochemical Sciences

JF - Trends in Biochemical Sciences

IS - 1

ER -

No more brain tangles with ΔNp73

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this