Journal of Science: Relationship between natural A-beta antibodies and alzheimer's brain amyloid and cognitive function

Alzheimer's disease (AD), commonly known as Alzheimer's disease, is a de-detox.
early stages, AD is characterized by aggregation and memory loss of amyloid β (A beta) and tau proteins in the brain.
15-20 years before AD attacks, toxic β-amyloid molecules accumulate in the patient's brain.
when a patient's consciousness is impaired, the neurons in his brain have died in large numbers, leading to brain atrophy.
this case, it is difficult to save dead neurons by using drugs to remove starch deposits or entanglements in nerve fibers.
A-beta is the core healing substance of AD, and A-beta deposits in the brain to form senile plaque is the main pathological change of AD.
immunotherapy for A-beta, including active immunity (A-beta vaccine) and passive immunity (A-beta antibody), has been shown to be effective in AD animal models.
clinical trials of AD immunotherapy are currently failing, one of the main causes of failure is the occurrence of side effects, the specific mechanism is not clear.
natural A-beta autoantibodies (NAbs-A beta) are widely present in humans, studies have shown that NAbs-A beta is antagonist to the neurotoxic effects of A-beta and protects AD.
Previously, research from Professor Wang Yanjiang of Neurology, Daping Hospital, Third Military Medical University, Chongqing, suggested that NAbs-A beta has the functional heterogeneity associated with the table, that is, mid-stage NAbs-A beta can significantly inhibit A-beta aggregation, antagonist A-beta neurotoxic effect, thus having neuroprotective effect; N-side NAbs-A beta can bind directly with neurons and promote the production of A-beta, promote neuron apoptosis; AD patients in the body A beta autoantibodies spectrum presents characteristic disorders, that is, the mid-stage NAbs-A beta ratio is relatively reduced and the N-end NAbs-A beta ratio is relatively high, A beta autoantibodies spectrum disorders may be involved in the occurrence and development of AD, at the same time has a certain clinical diagnostic value.
recently, Professor Wang Yanjiang's team further evaluated the relationship between NAbs-A beta and AD brain amyloid and cognitive function.
the results were published in the journal Science Advances.
the study is a cross-border study conducted simultaneously in China and Australia.
researchers recruited 91 patients with distributed AD from Daping Hospital in Chongqing.
control group (CN) who matched each other were randomly recruited from the Taiping Hospital Health Checkup Center.
, 40 participants in each group had waist-wearing cerebrospinal fluid (CSF).
, on the other hand, the Australian Imaging, Biomarker and Lifestyle (AIBL) study is a longitudinal study of age-related neuroimaging, biomarkers, and lifestyle.
focus on clinical and neuropsychological analysis.
72-month follow-up of participants recruited from the AIBL, at baselines of 18, 36, 54 and 72 months, respectively.
included 360 participants, including 210 A-PET-CN, 120A beta-PET-CN and 30 A-PET-AD patients.
results showed that the level of NAbs-A beta at the end of targeted A-beta in patient plasma and CSF increased significantly compared to that of CN subjects, while the level of targeted mid-range was significantly lower.
, the above-mentioned level changes were associated with higher brain amyloid degeneration at the patient baseline and faster cognitive decline during follow-up.
, the results show that disorders of the A-beta autoantibod spectrum may be involved in the occurrence and development of AD.
adaptive immune system changes dynamically during AD progress and is associated with current passive immunotherapy strategies.
: Liu YH, et al. Association of naturally occurring antibodies to β-amyloid with cognitive decline and cerebral amyloidosis in Alzheimer’s disease. Science Advances01 Jan 2021. DOI: 10.1126/sciadv.abb0457MedSci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that state "Source: Mets Medicine" or "Source: MedSci Originals" are owned by Mets Medical and are not authorized to be reproduced by any media, website or individual.
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