Back to "Research and Funding"


The non-profit NCL-Foundation is committed to collaborative research funding. In order to bring relevant NCL research projects to the forefront, we are continuously looking for suitable partners from both the profit and the non-profit sector. We are in close contact with other foundations, self-help groups and associations.


The funding landscape of the NCL Foundation. Projects are funded worldwide. Ongoing promotions are shown in red, the completed in yellow. (January 2015)

Promotion periods

Here you can download an overview of the periods of all projects promoted by the NCL Foundation, including their project supervisors.



How do we promote?

We encourage young scientists by awarding PhD fellowships.

In addition, the NCL Foundation periodically offers the NCL Research Award as a prize. With the prize money postdoctoral candidates are financially supported.

For more than 10 years, the Foundation brings research collaborations to the forefront and supports scientists in the implementation of their projects in the field of research into NCL. Click here for further information on the current promotions and the completed projects of the NCL Foundation.


The following publications have emerged so far from our funded projects: 























































  • "Retinal function in aging homozygous Cln3 (ex7/8) knock-in mice" (Link)

  • "Non-invasive assessment of retinal alterations in mouse models of infantile and juvenile neuronal ceroid lipofuscinosis by spectral domain optical coherence tomography" (Link)
  • "CLN3 deficient cells display defects in the ARF1-Cdc42 pathway and actin-dependent events" (Link)
  • "Human iPSC models of neuronal ceroid lipofuscinosis capture distinct effects of TPP1 and CLN3 mutations on the endocytic pathway" (Link)

  • "Partial correction of the CNS lysosomal storage defect in a mouse model of juvenile neuronal ceroid lipofuscinosis by neonatal CNS administration of an adeno-associated virus serotype rh.10 vector expressing the human CLN3 gene" (Link)

  • "Funding resources for rare disease research" (Link)
  • "Progressive Retinal Degeneration and Glial Activation in the CLN6 (nclf) Mouse Model of Neuronal Ceroid Lipofuscinosis: A Beneficial Effect of DHA and Curcumin Supplementation" (Link)
  • "Genetic basis and phenotypic correlations of the neuronal ceroid lipofusinoses" (Link)
  • "Lysosomal membrane permeability stimulates protein aggregate formation in neurons of a lysosomal disease" (Link)
  • "Immune cells perturb axons and impair neuronal survival in a mouse model of infantile neuronal ceroid lipofuscinosis" (Link)
  • "Large-scale phenotyping of an accurate genetic mouse model of JNCL identifies novel early pathology outside the central nervous system" (Link)
  • "The yeast Batten disease orthologue Btn1 controls endosome-Golgi retrograde transport via SNARE assembly" (Link)
  • Btn3 is a negative regulator of Btn2-mediated endosomal protein trafficking and prion curing in yeast (Link)

  • "Osmoregulation of ceroid neuronal lipofuscinosis type 3 in the renal medulla" (Link)
  • "[NCL in animal models]" (Link)
  • "[Juvenile neuronal ceroid lipofuscinosis. Ophthalmologic findings and differential diagnosis]" (Link)

  • "[Diagnostics and treatment of neuronal ceroid lipofuscinoses from the viewpoint of neuropediatricians]" (Link)

  • "[Genetics of neuronal ceroidlipofuscinoses. Aspects of genetic counseling]" (Link)

  • "Developmental impairments of select neurotransmitter systems in brains of Cln3 (Deltaex7/8) knock-in mice, an animal model of juvenile neuronal ceroid lipofuscinosis" (Link
  • "C-Terminal Prenylation of the CLN3 membrane glycoprotein is required for efficient endosomal sorting to lysosomes." (Link)
  • "Increased expression of lysosomal acid phosphatase in CLN3-defective cells and mouse brain tissue." (Link)
  • "[The role of the ophthalmologist in the management of juvenile neuronal ceroid lipofuscinosis]" (Link)

  • "A dileucine motif and a cluster of acidic amino acids in the second cytoplasmic domain of the batten disease-related CLN3 protein are required for efficient lysosomal targeting." (Link)


Contact Person

Dr. Herman van der Putten

Mobile: +49 (0) 163-7383083


This German - English translation was done by the translators Tizzy Mann, Andrea Murphy, Kate Humby and Marcia Neff for the PerMondo initiative that involves providing free translations for NGOs. PerMondo is sponsored and run by the translation agency Mondo Agit.