Recently, many papers have reported the physiological functions of
amyloid beta and
amyloid precursor
protein (APP). In particular, one of its functions is of importance for synaptic plasticity. Extracellular
amyloid beta may suppress synaptic plasticity or inhibit long-term potentiation (LTP) from outside the cell. LTP is now considered the molecular basis of memory.
Amyloid beta may induce the inhibition or loss of memory. We propose that suppression of LTP by
amyloid beta induces a kind of physiological forgetfulness. On the other hand,
homocysteic acid (HA) which is released from astrocytes under stress conditions accumulates the
amyloid beta into neuronal cell, which consequently induces the inhibition of
amyloid beta physiological function and induces strong LTP. We propose that HA induces strong unforgetful memory under stress condition such as
PTSD and emotional depression. The situation is different in the elderly people. Prolonged stress in the elderly people may induce
neurodegenerative diseases such as
Alzheimer's disease. We observed that in the presence of excess
methionine, HA induced
alpha-synuclein protein in cultured cells, suggesting a hypermethylation model in vivo. Usually hypermethylation is observed in the ageing process. We have shown that HA promotes the accumulation of
amyloid beta in cells, and that the production of
alpha-synuclein, which induces the aggregation of
amyloid beta, impairing the cell function. LTP is inhibited by deficient cellular function, which means that memories cannot be formed. In fact, there is
confusion of memories in the early stages of
Alzheimer's disease. Finally, the aggregated
alpha-synuclein induces tau pathology, which induces cell death, leading to Alzheimer's pathology. In conclusion, we propose that HA induces Alzheimer's pathology in the elderly people because of prolonged stress.