The Amyloid Precursor Protein (APP) is infamous for its role in Alzheimer’s disease (AD) due to overproduction of a small proteolytic APP breakdown product the amyloid β (Aβ). In contrast to this pathological role, Aβ (and other APP cleavage products) have significant functions in lipid homeostasis that, as recent clinical data suggest, might hold a clue for treatment of Alzheimer’s disease. Amyloid deposition is the first notable AD-linked pathology. With progression of the disease further synaptic and other cerebral pathologies accumulate. Studies performed in vitro and in AD-model animals suggest that multi-nutrient treatment would allow to synergistically target several of those pathologies as well as to enhance efficacy compared with individual nutrients. The aim was to provide neuroprotection by targeting disease processes in early AD, i.e., by supplying rate-limiting compounds for brain phospholipid synthesis and addressing multiple AD-related pathological processes in vivo. Studies in animal models showed that this multi-nutrient combination improved neuronal membrane composition, increased the formation of synapses, cholinergic neurotransmission, and cerebral blood flow and perfusion, preserved neuronal integrity, restored hippocampal neurogenesis, reduced β‑amyloid pathology, and improved cognition. For clinical use a specific multi-nutrient combination (Fortasyn Connect/FC) was used. The LipiDiDiet study is a 6-year (2 year with a blinded extension up to 4 years), double-blind, parallel-group, multi-country RCT in subjects with prodromal AD, receiving FC or an iso-caloric control product once daily. A total of 311 subjects with prodromal AD were randomized. Study product compliance was high and there were no reasons for safety concerns. Main results include favorable effects of the nutrient combination on the Clinical Dementia Rating (sum of boxes) and reduced brain atrophy. FINANCIAL SUPPORT: European Commission under the 7th framework programme of the European Union, Grant Agreement No. 211696. Additional funding was provided by the EU Joint Programme – Neurodegenerative Disease Research (JPND) (MIND-AD grant).
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