SCIENCE

Essential Fatty Acids and the Brain

Essential Fatty Acids (EFAs) and long-chain polyunsaturated fatty acids (PUFAs), such as docosahexaenoic acid (DHA) are lipids critical for brain growth, development and function.

However, the brain's protective blood brain barrier (BBB) is impermeable to free circulating EFAs or those bound to triglycerides and most phospholipids1,2. How the brain acquires its lipids during development and throughout life has remained a puzzle to scientist for years. 

 

The Discovery of MFSD2a and LPL-EFAs

  • To enter the brain, EFAs must be transported by a specific protein found on the BBB; the Major Facilitator Superfamily Domain–Containing 2a (MFSD2a)3-6
  • MFSD2a specifically transports EFAs and PUFAs attached to a Lysophospholipid (LPL), of which Lysophosphatidylcholines (LPCs) are the most abundant circulating form5.
  • Patients with genetic mutations in MFSD2a that disrupt LPC-EFA transport suffer from severe microcephaly (small brains) and cognitive defects3,4.
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These findings demonstrate that MFSD2a is the major transporter of EFAs to the brain during development and throughout life. In addition, LPLs are a previously under-appreciated pool of EFAs critical to brain growth and function in humans.

 

Vanteres’ preclinical and clinical research if focused on:

  • Identifying populations or conditions in which deficiencies or dysregulation of LPLs contribute to poor health and/or disease.
  • The development of specific ATLs as therapeutics for the treatment of these conditions.

 


SOLUTIONS

MFSD2a and ATLs – the Larger Opportunity  

MFSD2a transports LPL-unsaturated fatty acids, such as LPC-DHA, more efficiently than the more abundant LPL-saturated fatty acids5,6. At the level of the BBB and retinal-blood barrier (REB), this is consistent with MFSD2a preferential delivery of DHA to the brain and eye.

However, MFSD2a is also expressed in several tissues and cell types where EFA uptake does not require MFSD2a transport i.e. liver and brown adipose tissue5,6

Emerging science indicates that MFSD2a transport of LPL-EFAs can act as a intracellular signal to regulate cellular function, and that dysregulation of LPL-EFA metabolism, transport and/or signalling may contribute to disease. 

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Our current pipeline of ATLs is focused on four main benefit areas:

  • Cognition - Maternal Health/Early Cognitive Development
  • Metabolic disease – Unspecified Condition
  • Eye Health – Unspecified Condition
  • Unspecified Condition