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Related Experiment Video

Updated: May 8, 2026

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

Targeting synaptic dysfunction in Alzheimer's disease by administering a specific nutrient combination.

Nick van Wijk¹, Laus M Broersen, Martijn C de Wilde

¹Nutricia Advanced Medical Nutrition, Nutricia Research, Utrecht, The Netherlands.

Journal of Alzheimer'S Disease : JAD

|August 30, 2013

Summary

Early Alzheimer's disease (AD) involves synapse loss. A specific nutrient combination, Fortasyn Connect (FC), is designed to support neuronal membranes and has shown promise in improving memory function in mild AD patients.

Keywords:

Alzheimer's disease Fortasyn Connect Souvenaid amyloid-β membrane neurotransmission nutrition phospholipid synaptic dysfunction

Related Experiment Videos

Last Updated: May 8, 2026

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

Area of Science:

Neuroscience
Nutritional Science
Gerontology

Background:

Synapse loss and dysfunction are early pathological hallmarks of Alzheimer's disease (AD).
Neuronal and synaptic losses in AD are linked to degeneration and altered composition of neuronal membranes.
Membrane-related pathology and synapse loss represent viable therapeutic targets for AD intervention.

Purpose of the Study:

To review the scientific basis and preclinical evidence for Fortasyn Connect (FC), a nutrient combination designed to address nutritional needs in early AD.
To summarize the clinical findings supporting FC's potential to counteract synaptic loss and membrane pathology in AD.
To evaluate FC's efficacy in improving memory function and preserving brain network organization in mild AD.

Main Methods:

Review of basic scientific studies investigating the nutritional precursors and cofactors in FC.
Analysis of preclinical models examining FC's effects on neuronal membranes and synaptic function.
Summary of clinical study data on FC's impact on memory and functional brain network organization in mild AD.

Main Results:

FC comprises uridine, omega-3 fatty acids (DHA, EPA), choline, phospholipids, folic acid, B vitamins, and antioxidants.
Preclinical studies support the hypothesis that FC provides essential nutrients for neuronal membrane formation and function.
Clinical studies indicate that FC-containing medical food improves memory and preserves functional brain network organization in mild AD.

Conclusions:

FC is a targeted nutritional intervention designed to support neuronal membrane health and function in early AD.
The nutrient combination shows potential in counteracting synaptic dysfunction and improving cognitive outcomes in mild AD.
Further clinical validation supports FC as a strategy to address early AD-related memory deficits and synaptic pathology.