GLYCATION GLYCATION & COGNITION WHAT'S NEW?

Schizophrenia and longevity.

The impact of glycation on social behaviour.

Schizophrenia is a fairly common disabling psychiatric illness affecting around 1% of the population. Its diagnosis is often difficult and delayed, and is characterised by a wide range of symptoms.
Genetics and environment are suggested to explain schizophrenia, but the mechanisms by which it develops remain largely poorly understood.
Schizophrenics have an increased risk of developing chronic illnesses, and their life expectancy is 10 to 20 years shorter than that of the general population.

Various studies have shown a correlation between schizophrenia and glycation levels. For the first time, researchers have shown that the accumulation of pentosidine, an advanced glycation product (AGEs), is involved in deficits in social behaviour (based on a mouse social defeat stress model (1).
This finding suggests that an individual’s glycation level, which is directly linked to their sugar intake, could influence their social behaviour.

Although there is no evidence of a direct causal link between glycation and schizophrenia, it appears that glycation is an aggravating factor in schizophrenia, notably because of the metabolic disturbances it induces.
At this stage, everything indicates that controlling glycation, particularly through diet, could have a beneficial effect on mental health.

© AGE Breaker 03 2025

[Glycation is one of the major causes of aging. Resulting from the fixation of sugars on the proteins constituting the organism, glycation generates toxic compounds that cause cellular aging. Glycation is particularly involved in metabolic disorders, skin aging and cognitive decline.]
[AGE BREAKER, patented nutritional supplements, based on rosmarinic acid, recognized by aging specialists around the world for their properties to reverse the effects of glycation.]

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(1): MASADA, Mayuko, TORIUMI, Kazuya, SUZUKI, Kazuhiro, et al. Role of pentosidine accumulation in stress-induced social behavioral deficits. Neuroscience Letters, 2025, p. 138180.
https://doi.org/10.1016/j.neulet.2025.138180