2018
DOI: 10.1002/brb3.915
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Early fine motor impairment and behavioral dysfunction in (Thy‐1)‐h[A30P] alpha‐synuclein mice

Abstract: IntroductionIntraneuronal inclusions of alpha‐synuclein are commonly found in the brain of patients with Parkinson's disease and other α‐synucleinopathies. The correlation between alpha‐synuclein pathology and symptoms has been studied in various animal models. In (Thy‐1)‐h[A30P] alpha‐synuclein transgenic mice, behavioral and motor abnormalities were reported from 12 and 15 months, respectively. The aim of this study was to investigate whether these mice also display symptoms at earlier time points.MethodsWe … Show more

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Cited by 27 publications
(51 citation statements)
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“…We propose that neurons with chronic overexpression of human A30P aSyn can still maintain retrograde transport and collect aSyn aggregates in perinuclear accumulations (SAs). Indeed, in the A30P mice without PFF injection, basal aSyn pathology is mostly restricted to somatic accumulations (SAs, reminiscent of LBs) with only few dystrophic neurites (DNs, reminiscent of LNs), consistent with earlier studies [22]. These mice do not show a loss of dopaminergic somata in the substantia nigra, degeneration of dopaminergic axon terminals in the striatum or glial activation (Figs.…”
Section: Discussionsupporting
confidence: 89%
See 1 more Smart Citation
“…We propose that neurons with chronic overexpression of human A30P aSyn can still maintain retrograde transport and collect aSyn aggregates in perinuclear accumulations (SAs). Indeed, in the A30P mice without PFF injection, basal aSyn pathology is mostly restricted to somatic accumulations (SAs, reminiscent of LBs) with only few dystrophic neurites (DNs, reminiscent of LNs), consistent with earlier studies [22]. These mice do not show a loss of dopaminergic somata in the substantia nigra, degeneration of dopaminergic axon terminals in the striatum or glial activation (Figs.…”
Section: Discussionsupporting
confidence: 89%
“…These mice do not show a loss of dopaminergic somata in the substantia nigra, degeneration of dopaminergic axon terminals in the striatum or glial activation (Figs. 2B, 3A and reference [11]), but their neurons are vulnerable [13,[22][23][24].…”
Section: Discussionmentioning
confidence: 99%
“…The MCSF has since its conception over a decade ago, proven useful in a number of studies using adult rats (Karlsson et al, 2009; Roman et al, 2012; Momeni and Roman, 2014; Palm et al, 2014; Magara et al, 2015) and mice (Augustsson and Meyerson, 2004; Ekmark-Lewén et al, 2010; Ekmark-Lewén et al, 2018). More recently, studies examining adolescent rats (Palm et al, 2013; Berardo et al, 2016; Wille-Bille et al, 2017, 2018) and mice (Stringer et al, 2017) have started using the MCSF as well.…”
Section: Discussionmentioning
confidence: 99%
“…One of the most widely studied αSyn transgenic (tg) models expresses human αSyn (h-αSyn) containing the point mutation A30P, which has been found to cause PD in humans ( 11 ). The tg A30P αSyn mice present PD-like motor symptoms at around 8 months of age and there are abundant αSyn aggregates found throughout the brainstem and midbrain ( 12 15 ). The motor symptoms have been associated with an increase in soluble αSyn protofibrils in the spinal cord ( 16 ).…”
Section: Introductionmentioning
confidence: 99%