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Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases

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Published on: July 28, 2013

No more brain tangles with DeltaNp73.

Mark P Mattson¹, Uri Ashery

¹Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA. mattsonm@grc.nia.nih.gov

Trends in Biochemical Sciences

|November 15, 2008

Summary

This summary is machine-generated.

A new study shows that reduced levels of the p73 protein isoform, DeltaNp73, worsen Alzheimer's disease (AD) pathology and cognitive decline in mice. Increasing DeltaNp73 may offer a new therapeutic strategy for AD.

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Area of Science:

Neuroscience
Molecular Biology
Gerontology

Background:

Alzheimer's disease (AD) involves neuronal dysfunction and death.
Aberrant tau phosphorylation leads to neurofibrillary tangles in AD.
The role of p73 isoforms in AD pathogenesis is largely unexplored.

Purpose of the Study:

To investigate the neuroprotective role of the truncated p73 isoform, DeltaNp73, in Alzheimer's disease.
To establish a novel animal model for studying tau pathology in AD.

Main Methods:

Utilized aged mice with naturally reduced DeltaNp73 levels.
Induced amyloid pathology in mice to assess DeltaNp73's impact.
Evaluated tau pathology, neurofibrillary tangle formation, and cognitive deficits.

Main Results:

Reduced DeltaNp73 levels in aged mice correlated with increased tau pathology and cognitive deficits.
DeltaNp73 reduction exacerbated neurofibrillary tangle formation and neuron death in mice with amyloid pathology.
These results establish a new AD animal model.

Conclusions:

The truncated p73 isoform, DeltaNp73, exhibits a neuroprotective function in Alzheimer's disease.
Modulating DeltaNp73 levels presents a potential therapeutic avenue for AD.
Further research into DeltaNp73 inducers is warranted for AD treatment.