We work with our clients to deliver a range of Parkinson’s related contract research and consultancy services that are tailored to their individual requirements in terms of science, timelines and cost.
Atuka provides services in three broad categories
Additional information on the models offered by Atuka
Motor and Non-Motor
Reserpine or haloperidol treated ratIdeal in-vivo proof of concept / screening platform for test items with anti-parkinsonian potential. Both models carry strong face- and predictive-validity.
6-OHDA-lesioned rat (full or partial lesion)Available as bilateral or unilateral for acute or chronic studies.
AAV α-synuclein ratProgressive rat model with PD-relevant inclusion pathology in addition to dopamine deficits.
Rotarod, open-field, cylinder, beam, step test Atuka offers a wide range of behavioural tests suitable for assessing impact of symptomatic treatments.
High-dose L-DOPA-treated reserpine rat
A rapid screening tool for compounds with potential anti-dyskinetic action.
Chronic L-DOPA-treated 6-OHDA-lesion mouse or rat (full)
Examine the effect of your Test Item on established L-DOPA-induced dyskinesia following acute or repeated treatment.
De novo L-DOPA-treated 6-OHDA-lesion mouse or rat
examine the effect of your Test Item to prevent development of L-DOPA-induced dyskinesia when co-administered with L-DOPA in naïve 6-OHDA-lesioned animals.
AIMs, rotarod, open-field test
A variety of MPTP paradigms can be used to produce dopaminergic lesions of different severities for assessing putative disease modifying treatments in both ‘ protective’ (treat before and / or alongside MPTP) or ‘restorative’ (treat after MPTP-lesion is established) implementations. Systemic bilateral lesion and well-characterised model.
6-OHDA lesion rat (partial)
Partial bilateral or unilateral lesions are established using a variety of 6-OHDA paradigms to produce dopaminergic lesions of different severities for assessing putative disease modifying treatments in both ‘ protective’ (treat before and / or alongside 6-OHDA) or ‘restorative’ (treat after 6-OHDA-lesion is established) implementations. Wealth of behavioural measures and well-controlled lesion size are strengths of this model.
AAV α-synuclein rat
this groundbreaking model progressive degeneration rat model with PD-relevant inclusion pathology in addition to dopamine deficits that develop over a period of weeks. Well characterised implementations using 1:1, 1:3 or 1:10 titers for a range of disease stage modeling options.
Protection / restoration of normal behaviour
Same full range of behavioural measures as described for symptomatic and ‘side-effect’ indications.
MPTP-lesioned marmosetNew-World small primate model. Excellent for assessing anti-parkinsonian potential.
MPTP-lesioned macaque (early or advanced disease model)Old-World primate model. Gold-standard for translation of symptomatic potential prior to moving towards clinical trials.
Parkinsonism (mPRS), activity, mMAP, actical™Includes unique assessment of behaviour by a movement-disorder specialist neurologist.
Chronic L-DOPA treated MPTP-lesioned marmoset
New-World primate best used for studying effect of Test Item to prevent development of L-DOPA-induced dyskinesia (de novo) when co-administered with L-DOPA in naïve animals. Also ideal model for examining effects of treatment on L-DOPA-induced psychosis.
Chronic L-DOPA treated MPTP-lesioned macaque (advanced)
Old-World primate model. Gold-standard for examining effects of treatment on established dyskinesia and translation of potential into clinical trials. Optimal assessment of effect on chorea vs. dystonia.
Dyskinesia (mDRS), psychosis, impulse control disorder
Includes unique assessment of behaviour by a movement-disorder specialist neurologist using scales adapted from clinical equivalents for parkinsonism (UPDRS pt. III; NHPDysR), dyskinesia (UDysR; NHPDysR) and ON-time with troublesome dyskinesia (ON-time with disabling dyskinesia).
MPTP-lesioned macaque (early)
Old-World primate with well characterised MPTP paradigm and resulting dopaminergic lesion. Disease modifying treatments may be assessed in both ‘ protective’ (treat before and / or alongside MPTP) or ‘restorative’ (treat after MPTP-lesion is established) implementations.
AAV α-synuclein macaque
Targeted surgical delivery to substantia nigra produces progressive model with PD-like inclusions and α-synucleinopathy able to assess therapeutics aimed at preventing or reducing α-syn accumulation.
Protection / restoration of normal behaviour
Same full-range of assessments as detailed for symptomatic and ‘side-effect’ indications but includes assessment of behaviour by a movement-disorder specialist neurologist using scales adapted from the UPDRS and UDysR scale.
Imaging (PET, SPECT, MRI, CT), targeted surgical delivery (gene, drug, implant), microdialysis, DMPK (plasma, csf via LC-MS/MS)
Biogenic amines (HPLC), immunohistochemistry, multi-label confocal cell counting & fiber density stereology, receptor binding, gene microarray, multiplex ELISA (trophic factors, cytokines, etc ) , in-situ hybridisation, DMPK (tissue via LC-MS/MS)
Phase II trial design and execution