Dietary supplement of titrated extracts, with Coenzyme Q10 and Lactoferrin.
Centella asiatica and Bacopa monnieri may be useful in supporting memory and cognitive function, Green Tea possesses antioxidant action.
| Nutritional information | per maximum daily serving (1 stick) |
| Turmeric ES Tit. 95% of which curcuminoids |
1200 mg 1140 mg |
| Bacopa ES Tit. 20% of which bacosides |
500 mg 100 mg |
| Ashwagandha ES Tit. 2.5% of which withanolides |
500 mg 12.5 mg |
| Centella ES Tit. 20% of which asiaticoside |
500 mg 100 mg |
| Green Tea ES. 95% of which polyphenols of which EGCG |
200 mg 190 mg 60 mg |
| Coenzyme Q10 | 100 mg |
| Black pepper ES Tit. 95% of which piperine |
1 mg 0.95 mg |
| Lactoferrin | 100 mg |
Water; Cocoa butter; Turmeric (Curcuma longa L.) rhizome ES tit. 95% in curcuminoids; Bacopa (Bacopa monnieri (L.) Pennell) aerial part ES tit. 20% in bacosides; Ashwagandha (Withania somnifera (L.) Dunal.) root ES tit. 2.5% in withanolides; Centella (Centella asiatica (L.) Urb.) aerial part ES tit. 20% in asiaticoside; Antioxidant: Ascorbic acid; Acidity corrector: Sodium lactate; Green Tea (Camellia sinensis (L.) Kuntze) leaves ES tit. 95% in polyphenols and 30% in (-)-epigallocatechin-3-gallate (EGCG); Acidifier: Citric acid; Lactoferrin (milk derivative); Coenzyme Q10; Thickener: Xanthan gum; Preservative: Potassium sorbate; Sweetener: Sucralose; Emulsifier: Soy Lecithin; Flavor; Black pepper (Piper nigrum L.) fruits ES tit. 95% in piperine.
30 12 ml monodies sticks.
Coping with changes in the nervous system does not mean losing, but discovering new ways of listening to oneself. For many, the beginning is subtle: concentration becomes more selective, memory requires more attention, thoughts take their own time to form. It is a process that may advance slowly, but it does not shut down the mind: it guides it to different rhythms. Even when entering the territory of neurodegenerative diseases, daily living can continue to accommodate gestures full of meaning, expressions of presence, and authentic relationships.
Cognitive decline is not a barrier, but a transformation of experience. Orientation may change, language may slow down, but curiosity, sensitivity, the need to express oneself remain. Those who observe these changes closely also discover new ways of being around, of communicating with more empathy, of finding value in small things. Habitual activities change, it is true, but they continue to exist, perhaps with more simplicity, more gentleness, less haste.
In cellular tissue, energy availability is reduced, and the brain adapts intelligently, learning to distribute resources where they are really needed. Renewal mechanisms become less efficient, but they do not stop: they slow down, rebalance, and ask for more time to run their course. Even neuroinflammation, now increasingly understood, is not a judgment, but a challenge that can be addressed with innovative approaches and personalized strategies.
Changes in mood and attention, as well as small changes in movement, are valuable signals. They speak of a nervous system that continues to communicate, to seek balance, to respond to stimuli in new ways. Even in cases of atypical parkinsonism or motor slowing, adaptation remains possible, and the body finds alternative forms of expression and coordination.
Those who go through this experience do not lose themselves, but rediscover their inner selves through a different lens. Words may take longer, thoughts may follow slower trajectories, but each passage remains an act of presence. It is a profound journey of sensitivity and rediscovery in which the mind, even as it changes, continues to speak, to feel, to connect. And it is in this new harmony that space opens up for a life that is still full, aware and intensely human.
Neurodegenerative diseases result from a complex interplay of molecular, systemic, and behavioral factors that profoundly alter the homeostasis of the central nervous system. Underlying these processes is often a progressive impairment of intracellular mechanisms responsible for maintaining neurophysiological balance. Among the first detectable alterations is the malfunction of the autophagic pathway, a system responsible for the degradation and recycling of damaged cellular components. When this mechanism breaks down or slows down, there is an accumulation of protein aggregates that interferes with synaptic activity, hindering communication between neurons and triggering a vicious cycle of progressive degeneration.
In parallel, mitochondrial dysfunction impairs energy production at the neuronal level, reducing ATP availability and increasing the production of reactive oxygen species. This imbalance promotes theestablishment of a state of chronic oxidative stress, a condition that damages cell membranes, alters gene expression, and accelerates apoptotic processes. Cumulative damage to mitochondria further exacerbates the ability of nerve cells to maintain their functions, making brain tissue increasingly vulnerable.
Added to these mechanisms is neuroinflammation, a process involving chronic activation of microglia and astrocytes. This immune response, initially protective, in the presence of a persistent stimulus becomes a destabilizing factor, exacerbating neuronal damage and contributing to the amplification of the inflammatory cascade. The persistence of inflammatory signals in the neuronal microenvironment alters synaptic plasticity, slows learning and memory processes, and impairs the nervous system's ability to respond adaptively to stimuli.
These events, while initially silent, develop over a long and often asymptomatic time span, making early recognition difficult. However, their cumulative impact creates a favorable biological terrain for the onset and progression of neurodegenerative diseases. The interplay between alteration of the autophagy pathway, accumulation of protein aggregates, mitochondrial dysfunction, oxidative stress, and neuroinflammation represents a complex pathophysiological network, which requires focused attention and an integrated view to understand its scope and act early in protecting the nervous system.
Alibrain offers an integrative strategy for for the overall well-being of the nervous system; it stands as a nonpharmacological adjunct to help manage situations in which neuroinflammation and alterations in endogenous antioxidant systems occur, taking into account the complexity of these situations and the challenges posed by conventional therapies in terms of side effects or limited long-term efficacy in modifying disease evolution.
Antioxidant activity represents one of the pivotal mechanisms of Alibrain's efficacy.
The plant actives in the formulation counteract the accumulation of free radicals, reducing oxidative damage at the level of cell membranes and the most sensitive intracellular structures. In parallel, theanti-inflammatory activity helps modulate the neuroinflammatory cascade that often accompanies neurodegenerative processes.
Alibrain acts in supporting mitochondrial function by promoting the efficiency of ATP production and contributing to the stability of membrane potential, which is essential for synaptic transmission. This effect is complemented by the ability to regulate cell clearance systems, with particular reference to the activation of autophagy, a process essential for the recycling of damaged components and the maintenance of long-term neuronal function.
The plant extracts in Alibrain also play a specific action in counteracting protein aggregation, the accumulations of which are implicated in neurodegenerative disorders, particularly parkinsonisms.
The synergy of the selected active ingredients makes Alibrain an effective ally in supporting the nervous system, thanks to acomprehensive neuroprotective action geared toward preventing neuronal damage. A refined intervention designed to protect cognitive function over time and effectively accompany the brain's natural processes of adaptation and regeneration.
The patented Lacursome® technology uses lipid nanoparticles that, thanks to Lactoferrin, are able to bind to receptors on the blood-brain barrier, delivering active ingredients directly into the central nervous system and improving their absorption and availability.
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