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

^*Corresponding author for this work

Department of Neurobiology

National Institutes of Health

Research output: Contribution to journal › Short survey › peer-review

7 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
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

Funding

Funders	Funder number
National Institute on Aging	ZIAAG000312

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

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10.1016/j.tibs.2008.10.004

Cite this

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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.",

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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.

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No more brain tangles with ΔNp73

Abstract

Funding

UN SDGs

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