Evidence map›Paper›PMID 37694372›Full record

ArticleJournal of Huntington's disease2023

Age-Dependent Increase in Tau Phosphorylation at Serine 396 in Huntington's Disease Prefrontal Cortex.

Tiziana Petrozziello, Sommer S Huntress, Ayleen L Castillo-Torres, James P Quinn, Theresa R Connors, Corinne A Auger, Alexandra N Mills, Spencer E Kim, Sophia Liu, Farah Mahmood and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Huntington's disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Mild cognitive impairment in Huntington's disease: challenges and outlooks.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 3 institutions in 2 countries.

Tiziana PetrozzielloSean M. Healey & AMG Center for ALS at Mass General, MassGeneral Brigham, Boston, MA, USA.
Sommer S HuntressSean M. Healey & AMG Center for ALS at Mass General, MassGeneral Brigham, Boston, MA, USA.
Ayleen L Castillo-TorresSean M. Healey & AMG Center for ALS at Mass General, MassGeneral Brigham, Boston, MA, USA.
James P QuinnDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Theresa R ConnorsDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Corinne A AugerDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Alexandra N MillsSean M. Healey & AMG Center for ALS at Mass General, MassGeneral Brigham, Boston, MA, USA.
Spencer E KimSean M. Healey & AMG Center for ALS at Mass General, MassGeneral Brigham, Boston, MA, USA.
Sophia LiuDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Farah MahmoodDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Adel BoudiDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Muzhou WuCenter for Genomic Medicine, MassGeneral Brigham, Boston, MA, USA.
Ellen SappDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Pia KivisäkkDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Shekar R SundereshDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Mahmoud A PouladiDepartment of Medical Genetics, Centre for Molecular Medicine and Therapeutics, British Columbia Children's Hospital Research Institute, University of British Columbia, Vancouver, Canada.
Steven E ArnoldDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Bradley T HymanDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
H Diana RosasDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Marian DiFigliaDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Ricardo Mouro PintoDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Kimberly Kegel-GleasonDepartment of Neurology, MassGeneral Brigham, Boston, MA, USA.
Ghazaleh Sadri-VakiliSean M. Healey & AMG Center for ALS at Mass General, MassGeneral Brigham, Boston, MA, USA.
MaineGeneral Medical Center · USHarvard University · USUniversity of British Columbia · CA

Funding

Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI STEVEN E ARNOLD · 2019 to 2026
$36.5M
Somatic Repeat Expansions as a Therapeutic Target for Trinucleotide Repeat DisordersR01NS126420 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI Ricardo Mouro Pinto · 2022 to 2026
$2.0M
NIA NIH HHS P30 AG062421NINDS NIH HHS R01 NS126420
6 · The paper itself

Abstract

backgroundTo date, it is still controversial whether tau phosphorylation plays a role in Huntington's disease (HD), as previous studies demonstrated either no alterations or increases in phosphorylated tau (pTau) in HD postmortem brain and mouse models.

objectiveThe goal of this study was to determine whether total tau and pTau levels are altered in HD.

methodsImmunohistochemistry, cellular fractionations, and western blots were used to measure total tau and pTau levels in a large cohort of HD and control postmortem prefrontal cortex (PFC). Furthermore, western blots were performed to assess tau, and pTau levels in HD and control isogenic embryonic stem cell (ESC)-derived cortical neurons and neuronal stem cells (NSCs). Similarly, western blots were used to assess tau and pTau levels in HttQ111 and transgenic R6/2 mice. Lastly, total tau levels were assessed in HD and healthy control plasma using Quanterix Simoa assay.

resultsOur results revealed that, while there was no difference in total tau or pTau levels in HD PFC compared to controls, the levels of tau phosphorylated at S396 were increased in PFC samples from HD patients 60 years or older at time of death. Additionally, tau and pTau levels were not changed in HD ESC-derived cortical neurons and NSCs. Similarly, total tau or pTau levels were not altered in HttQ111 and transgenic R6/2 mice compared to wild-type littermates. Lastly, tau levels were not changed in plasma from a small cohort of HD patients compared to controls.

conclusionsTogether these findings demonstrate that pTau-S396 levels increase significantly with age in HD PFC.

Indexed as

Huntington DiseaseAnimalsDisease Models, AnimalHumansMiceMice, TransgenicPhosphorylationPrefrontal CortexSerineSerineESC-derived neuronsfractionationsHuntington’s diseasemouse modelsneuronal stem cellsphosphorylated tauplasmapostmortem braintotal tau

Identifiers

PMID37694372
PMCPMC11823699
OpenAlexW4386465547

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.