Towards an Immortal Brain


[   C  H  R  O  N  I  C  L  E   ]


Immortality and eternal youth are recurring themes in human culture. Although our species may have pushed back the limits of longevity, it always comes up against the finality of life. Ageing is an inevitable consequence of life and is expressed in the gradual decline of tissues, organ function and an increased risk of mortality. But why do we age? Our knowledge of the underlying biological processes is far from realising our dreams of eternal life.

A model established in 2015 suggests that ageing operates on four levels, from the molecular to the body as a whole, via the cellular and physiological control systems. Dysfunction in each layer and in their interconnections would explain the lines of age and the susceptibility to disease. On the molecular level, aging is thus associated with genetic and epigenetic changes (that modify the expression of genes without changing their code). The genetic modifications sometimes come with alterations in cell function, causing them to die or to proliferate.

On a larger scale, failures related to aging can increase the risk of developing chronic inflammation, deregulation of the metabolism or of the endocrine system. Then the body as a whole suffers functional decline, and develops cancers, cardiovascular, metabolic and neurodegenerative diseases. Thus, we know that normal aging of the brain is linked to relatively subtle changes at the synapses (contact points between neurons) in regions like the hippocampus and the prefrontal cortex. Studies in animals have identified cellular and synaptic changes in these brain structures during aging and which are likely directly linked to cognitive decline. We also know that “successful” aging is partly determined by factors associated with lifestyle and culture – a limited diet and physical activity in particular have a neuroprotective action that we are only just beginning to understand. According to recent work, there is a bi-directional relationship between the consumption of energy and nerve cell function. A low-calorie diet helps to lastingly strengthen synaptic contacts, a potentially fundamental mechanism in learning and memory. It can also affect the production of new neurons. On the contrary, excessive food consumption endangers these processes and accelerates brain aging, as in the case of diabetes and obesity. How this strategy can be implemented however remains to be studied, as it depends on many factors. It is not a question of depriving oneself of food to age better! Physical and mental activities also help to protect neurons against the failures linked to age through a variety of mechanisms, such as increasing neurotrophic factors (small proteins that help to develop and remodel neuronal networks), improving synaptic plasticity and stimulating the production of neurons.

Other treatment strategies are offering interesting possibilities. An anti-diabetic molecule for example, metformine, has a protective effect on the brain and acts by limiting the quantity of glucose metabolised. Also, a “parabiosis” experiment, combining the blood circulation of two mice, one elderly and the other young, led to the identification of GDF11, a neuroprotective molecule present in young mice (see here and here). Although a human application remains far off, this work suggests that, without necessarily becoming eternal, we may be able to limit the consequences of aging on memory and cognition and identify potential targets for the treatment and prevention of neurodegenerative diseases.






Mariana Alonso


Mariana Alonso is a neuroscientist at the Laboratory of Perception and Memory at Institut Pasteur. Her work looks into neurogenesis and brain plasticity in adults, the neuronal bases of smell linked to behaviour and the relationships between the microbiota, immunity and the brain. 

Share on Facebook
Share on Twitter
Please reload


November 11, 2018

November 11, 2018

Please reload