[Surrogate marker for ABeta42].
Currently, therapeutic intervention for Alzheimer disease (AD) after the disease onset is not very effective because progressive neuronal death precedes clinical symptoms. Available medicines such as AchE inhibitors transiently slow the progression of the symptoms, but they do not inhibit the pathological process. On the other hand, most of the next generation anti-AD drugs under development in pharmaceutical companies are to function to inhibit the progress of the pathological process and, thus, establishment of highly probable prediction of AD onset is necessary. AD is diagnosed using clinical criteria coupled with brain imaging systems such as SPECT and PET. To diagnose AD cases before the onset, it will be necessary to develop methods for detecting the pathological accumulation of proteins (e.g., Abeta in the brain, or develop biomarkers for predicting Abeta/tau accumulation in the brain. Our recent discovery of APL1beta28, a possible biomarker of AD, may contribute to early detection of AD.
Okochi
Masayasu
M
Psychiatry Department of Integrated Medicine, Division of Internal Medicine, Osaka University Graduate School of Medicine, Suita, Japan. masaokochi@gmail.com
Tagami
Shinji
S
Yanagida
Kanta
K
Takeda
Masatoshi
M
D000544:Alzheimer Disease / Q000175:diagnosis*; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor / Q000032:analysis*; D015415:Biomarkers / Q000032:analysis; D001921:Brain / Q000378:metabolism*; D015195:Drug Design; D042241:Early Diagnosis; D006801:Humans; D010446:Peptide Fragments
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D015415:Biomarkers; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)