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Synaptophysis is a core pathophysiological event of Alzheimer's disease (AD).
Synaptosis is associated with greater cognitive decline in Alzheimer's disease
than amyloid plaque pathology.
Other neurodegenerative diseases, including frontotemporal degeneration (FTLD) and Lewy body spectrum (LBD), are also characterized
by synaptic dysfunction and degeneration.
Since the first research to detect synaptic proteins in cerebrospinal fluid (CSF) appeared in the 90s of the 20th century, various synaptic proteins have been studied as potential biomarkers, and several methods
have been developed to quantify them.
Recently, experts from the University of Gothenburg, Sweden, have been concerned about Alzheimer's disease (AD; n = 63), frontotemporal lobe degeneration (FTLD; n = 53) and Lewy body spectrum (LBD; n = 21) patients and healthy control group (HC; n = 48) of the pathologically confirmed 17 synaptic proteins in the cerebrospinal fluid were quantified
.
The results showed that the comparison showed four different patterns: markers of all neurodegenerative diseases decreased compared to HC (neuronal pentraxins), markers of all neurodegenerative diseases increased (14-3-3 zeta/delta), markers of AD were selectively increased (neurogranin and β-synuclein) compared to other neurodegenerative diseases, compared with HC and AD, Markers of LBD and FTLD are selectively reduced (AP2B1 and synaxin-1B).
In summary, some synaptic proteins can be used as biomarkers of synaptic dysfunction in AD, LBD and FTLD
.
In addition, different patterns of synaptic protein alterations appear to be present in
various neurodegenerative diseases.
References:
Cerebrospinal fluid biomarker panel of synaptic dysfunction in Alzheimer's disease and other neurodegenerative disorders.
https://doi.
org/10.
1002/alz.
12809