Affiliations: [a] Alzheimer Center Limburg, School for Mental Health and Neuroscience (MHeNS), Maastricht University, Maastricht, the Netherlands
| [b] Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Department of Radiology, Charlestown, MA, USA
| [c] Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA
| [d] Faculty of Health, Medicine and Life Sciences; School for Mental Health and Neuroscience, Department of Psychiatry and Neuropsychology, Maastricht University, Maastricht, the Netherlands
Correspondence:
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Correspondence to: Joost M. Riphagen, MD, PhD, Faculty of Health, Medicine and Life Sciences; School for Mental Health and Neuroscience, Department of Psychiatry and Neuropsychology, Alzheimer Center Limburg, Maastricht University, Dr. Tanslaan 12, 6229 ET Maastricht, the Netherlands. E-mail: jriph@yahoo.co.uk.
Abstract: The brain-derived neurotropic growth factor (BDNF) gene has been linked to dementia, inflammation, and Apolipoprotein E (APOE) ɛ4 status. We used cerebrospinal fluid (CSF) amyloid-β (Aβ)42 and phosphorylated tau (p-tau) to investigate associations with BDNF polymorphisms and modifications by APOE ɛ4 or inflammation in a memory clinic population (n = 114; subjective cognitive decline, mild cognitive impairment, Alzheimer’s disease). We found distinct pathways to Alzheimer’s disease pathology: Val-Met displayed lower CSF-Aβ42 in APOE ɛ4+ carriers, independent of p-tau, while Val-Val displayed greater p-tau at higher IL-6 and sub-threshold Aβ42. This may contribute to resolving some inconsistencies in the BDNF literature and provide possible inroads to specific Aβ and tau interventions depending on BDNF polymorphism.
