Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Exacerbated synucleinopathy in mice expressing A53T SNCA on a Snca null background.

Neurobiology of aging - 1 Jan 2005

Cabin Deborah E, Gispert-Sanchez Suzana, Murphy Diane, Auburger Georg, Myers Robert R, Nussbaum Robert L

Abstract excerpt

Alpha-Synuclein is a major component of Lewy bodies, neuronal inclusions diagnostic for Parkinson's disease (PD). While an Ala53Thr mutation in alpha-synuclein can cause PD in humans, in mice the wildtype residue at position 53 is threonine, indicating that mice are either too short-lived to develop PD, or are protected by the six other amino acid differences between the proteins in these two species. Mice...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to alpha-Synuclein
Share to Glial Fibrillary Acidic Protein

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Microscopy, Electron, Transmission

Share to Phenylenediamines

Share to Sciatic Nerve

Share to Spinal Cord

Share to Synucleins

Share to Threonine

Source

Identifiers

PMID: 15585343
DOI: 10.1016/j.neurobiolaging.2004.02.026

Genes

SNCA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Exacerbated synucleinopathy in mice expressing A53T SNCA on a Snca null background.PMID 15585343Read ↗

Mouse models of alpha-synucleinopathy and Lewy pathology.Semantic proximity Read ↗

Neuronal alpha-synucleinopathy with severe movement disorder in mice expressing A53T human alpha-synuclein.Semantic proximity Read ↗

Neuropathology in mice expressing human alpha-synuclein.Semantic proximity Read ↗

Human alpha-synuclein-harboring familial Parkinson's disease-linked Ala-53 --> Thr mutation causes neurodegenerative disease with alpha-synuclein aggregation in transgenic mice.Semantic proximity Read ↗

Motor deficits and brain pathology in the Parkinson’s disease mouse model hA53TtgSemantic proximity Read ↗

Neuropathology in Mice Expressing Human α-SynucleinSemantic proximity Read ↗

Transgenic mice expressing mutant A53T human alpha-synuclein show neuronal dysfunction in the absence of aggregate formation.Semantic proximity Read ↗

Two C-terminal sequence variations determine differential neurotoxicity between human and mouse α-synucleinSemantic proximity Read ↗

Parkinson's disease alpha-synuclein transgenic mice develop neuronal mitochondrial degeneration and cell death.Semantic proximity Read ↗

Behavioural and dopaminergic changes in double mutated human A30P*A53T alpha-synuclein transgenic mouse model of Parkinson´s diseaseSemantic proximity Read ↗

Transgenic mice with human mutant genes causing Parkinson's disease and amyotrophic lateral sclerosis provide common insight into mechanisms of motor neuron selective vulnerability to degeneration.Semantic proximity Read ↗

Synphilin-1 attenuates neuronal degeneration in the A53T -synuclein transgenic mouse modelSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.