Matrix interaction
Determine how peptide intervention changes CSPG-associated binding and receptor engagement.
Research
Neural repair is constrained by the extracellular environment.
Maak studies how injury-induced proteoglycan signalling influences axonal growth, cellular repair and remyelination—and how peptide intervention can change that response.
Biological context
CSPG accumulation creates a persistent barrier to regeneration.
Following injury to the central or peripheral nervous system, chondroitin sulfate proteoglycans increase within reactive tissue and the extracellular matrix. Their glycosaminoglycan chains engage neuronal receptors, including protein tyrosine phosphatase sigma (PTPσ), and suppress growth-cone advance, axonal extension and plasticity.
This biology is relevant beyond the initial lesion. CSPG-rich environments also affect glial responses, remyelination and immune-cell behaviour, placing the matrix–receptor interface at an important point in the repair process.
Proteoglycan signalling
PTPσ distinguishes growth-promoting and growth-inhibiting matrix signals.
Heparan sulfate and chondroitin sulfate proteoglycans bind a common region of PTPσ but organise the receptor differently. HSPG-driven clustering is associated with neuronal extension; CSPGs disrupt that organisation and favour growth inhibition. This molecular switch provides a defined point for therapeutic investigation.
Research questions
From matrix interaction
to functional repair.
Maak concentrates on measurable biology that can connect molecular activity with a meaningful neural response.
Neurite growth
Measure growth-cone behaviour and neurite extension under defined inhibitory conditions.
Cellular repair
Study neuronal survival, glial responses and remyelination-related biology.
Translation
Connect exposure and biomarkers with anatomical, electrophysiological and functional outcomes.
Peptide precedent
The matrix–PTPσ axis is experimentally tractable.
Independent studies have shown that peptide approaches can reverse CSPG-associated neurite inhibition at the extracellular matrix and modulate PTPσ signalling at the receptor. Subsequent work has extended this biology into models of axonal repair, remyelination and functional recovery.
Maak uses this peer-reviewed foundation to define proprietary research programmes with their own molecular, cellular and translational work packages.
Explore MK-1Selected literature
Primary studies informing Maak's research field.
Science · 2009PTPσ is a receptor for chondroitin sulfate proteoglycan, an inhibitor of neural regeneration.Science · 2011Proteoglycan-specific molecular switch for RPTPσ clustering and neuronal extension.Nature · 2015Modulation of the proteoglycan receptor PTPσ promotes recovery after spinal cord injury.Frontiers in Cellular Neuroscience · 2022Low-Molecular Weight Protamine Overcomes Chondroitin Sulfate Inhibition of Neural Regeneration.Neuropharmacology · 2025Low-molecular weight protamine enhances neuroprotection and remyelination by mitigating chondroitin sulfate proteoglycan inhibition in models of demyelination.
Work with Maak