Researchers have largely focused on the accumulation of abnormal aggregates
of the beta-amyloid and tau proteins in the brain as causal factors in the
development of Alzheimer’s disease, but treatments targeting these protein
aggregates have shown limited success.
Individuals with Alzheimer’s disease show several metabolic changes
in the brain, including lower glucose (sugar) metabolism and depletion of
energy stores in cells, before the appearance of these protein aggregates.
A recent review suggests that high levels of fructose, particularly those
derived from added sugars, such as sucrose and high-fructose corn syrup,
could alter brain metabolism and cause degeneration of brain regions
associated with Alzheimer’s disease.Further studies are needed to establish the link between fructose and
Alzheimer’s disease, and evidence supporting this hypothesis could lead to
the development of strategies for the treatment or prevention of this
neurodegenerative condition.
The formation of abnormal aggregates of the beta-amyloid and tau
proteins are hallmarks of Alzheimer’s disease. However, treatments
targeting these abnormal protein aggregates have shown limited success.Instead, some researchers have proposed that alterations in brain
metabolism that appear prior to these protein aggregates may be responsible
for the development.
of the beta-amyloid and tau proteins in the brain as causal factors in the
development of Alzheimer’s disease, but treatments targeting these protein
aggregates have shown limited success.
Individuals with Alzheimer’s disease show several metabolic changes
in the brain, including lower glucose (sugar) metabolism and depletion of
energy stores in cells, before the appearance of these protein aggregates.
A recent review suggests that high levels of fructose, particularly those
derived from added sugars, such as sucrose and high-fructose corn syrup,
could alter brain metabolism and cause degeneration of brain regions
associated with Alzheimer’s disease.Further studies are needed to establish the link between fructose and
Alzheimer’s disease, and evidence supporting this hypothesis could lead to
the development of strategies for the treatment or prevention of this
neurodegenerative condition.
The formation of abnormal aggregates of the beta-amyloid and tau
proteins are hallmarks of Alzheimer’s disease. However, treatments
targeting these abnormal protein aggregates have shown limited success.Instead, some researchers have proposed that alterations in brain
metabolism that appear prior to these protein aggregates may be responsible
for the development.
