» Articles » PMID: 15717027

Using Advances in Neuroimaging to Detect, Understand, and Monitor Disease Progression in Huntington's Disease

Overview
Journal NeuroRx
Specialty Neurology
Date 2005 Feb 18
PMID 15717027
Citations 19
Authors
Affiliations
Soon will be listed here.
Abstract

Transgenic mouse models and other screens are being used to identify potential therapeutic agents for use in clinical trials in Huntington's disease (HD). The development of surrogate markers that can be used in clinical therapeutics is an active area of research. Because HD is relatively uncommon and only a portion of available subjects meet inclusion and exclusion criteria, therapeutic trials are limited by the availability of potential subjects as well as the relative insensitivity of the clinical measures used. Neuroimaging methods offer the potential to provide noninvasive, reproducible, and objective methods not only to better understand the disease process but also to follow in clinical studies to determine if a drug is effective in slowing down disease progression or perhaps even in delaying onset. Following is a review of the literature, which highlights the studies that have been published to date.

Citing Articles

How is Big Data reshaping preclinical aging research?.

Fernandez M, Martinez-Romero J, Aon M, Bernier M, Price N, de Cabo R Lab Anim (NY). 2023; 52(12):289-314.

PMID: 38017182 DOI: 10.1038/s41684-023-01286-y.


Assistive Technology for Cognition and Health-related Quality of Life in Huntington's Disease.

van Walsem M, Howe E, Frich J, Andelic N J Huntingtons Dis. 2016; 5(3):261-270.

PMID: 27689618 PMC: 5088402. DOI: 10.3233/JHD-160210.


BDNF-TrkB signaling in striatopallidal neurons controls inhibition of locomotor behavior.

Besusso D, Geibel M, Kramer D, Schneider T, Pendolino V, Picconi B Nat Commun. 2013; 4:2031.

PMID: 23774276 PMC: 3940866. DOI: 10.1038/ncomms3031.


Monitoring Huntington's disease progression through preclinical and early stages.

Tang C, Feigin A Neurodegener Dis Manag. 2012; 2(4):421-435.

PMID: 23243467 PMC: 3519443. DOI: 10.2217/nmt.12.34.


Tissue transglutaminase overexpression does not modify the disease phenotype of the R6/2 mouse model of Huntington's disease.

Kumar A, Kneynsberg A, Tucholski J, Perry G, van Groen T, Detloff P Exp Neurol. 2012; 237(1):78-89.

PMID: 22698685 PMC: 3418489. DOI: 10.1016/j.expneurol.2012.05.015.


References
1.
Mazziotta J, Phelps M, Pahl J, Huang S, Baxter L, Riege W . Reduced cerebral glucose metabolism in asymptomatic subjects at risk for Huntington's disease. N Engl J Med. 1987; 316(7):357-62. DOI: 10.1056/NEJM198702123160701. View

2.
Pavese N, Andrews T, Brooks D, Ho A, Rosser A, Barker R . Progressive striatal and cortical dopamine receptor dysfunction in Huntington's disease: a PET study. Brain. 2003; 126(Pt 5):1127-35. DOI: 10.1093/brain/awg119. View

3.
Aylward E, Codori A, Rosenblatt A, Sherr M, Brandt J, Stine O . Rate of caudate atrophy in presymptomatic and symptomatic stages of Huntington's disease. Mov Disord. 2000; 15(3):552-60. DOI: 10.1002/1531-8257(200005)15:3<552::AID-MDS1020>3.0.CO;2-P. View

4.
Kuwert T, Lange H, Langen K, Herzog H, Aulich A, Feinendegen L . Cortical and subcortical glucose consumption measured by PET in patients with Huntington's disease. Brain. 1990; 113 ( Pt 5):1405-23. DOI: 10.1093/brain/113.5.1405. View

5.
Reddy P, Williams M, Charles V, Garrett L, Whetsell Jr W, Miller G . Behavioural abnormalities and selective neuronal loss in HD transgenic mice expressing mutated full-length HD cDNA. Nat Genet. 1998; 20(2):198-202. DOI: 10.1038/2510. View