JNNP: Cerebrospinal fluid β-synactin can be used as an early diagnostic indicator of Alzheimer's disease

For Alzheimer's disease (AD), the testing of tau protein and amyloid β peptide (A beta 42) in cerebrospinal fluid (CSF) has been successfully applied to current diagnostic standards and clinical applications, but neither tau as a general marker of neurodegenerative degeneration nor a beta 42 as a marker of amyloid protein deposition can reflect degenerative changes in AD.
to assess synapse loss, which play a major role in AD pathogenesis, is important not only for AD diagnosis, but also for monitoring the effects of new drug candidates on synactal integrity in clinical trials.
addition, synapse loss often predests neuron degeneration and strikes early AD patients, even those with mild cognitive impairment (MCI).
, synhap loss was associated with a higher association with deterioration of cognitive function than plaque pathology.
, monitoring the loss of synactin released into cerebrospinal fluid is important for early diagnosis and/or prognosis.
β-synuclein with α-synuclein, with α-synuclein and γ-synuclein belong to the synuclein family.
β-synaptic nucleoproteins are found mainly in the brain and, more specifically, in the hypothyroids, the small brain, the neocute, the hippocupus, and the synapses.
is concentrated at the front end of the synapse and appears to play a role in membrane-related processes.
Because the new cortical glutamate energy cone neurons form cortisol, together with cortisol in the inner olfactory region and the hippoclic CA1 region, it is particularly easy to gather excessive phosphate tau, the formation of neurogenic fiber tangles and cell death, the study of whether the β-synaptic nucleoprotein is positioned in glutamate energy synapses is an important research topic.
paper reports on the establishment and validation β a new method of detecting the sandwich ELISA of the analytic-synth nucleoprotein.
, this paper analyzed seven different diagnostic groups: a total of 393 patients from four different clinical centers were analyzed for cerebrospinal fluid.
, β-synth nucleoproteins in brain tissue in 7 AD patients and 12 normal controls were tested, confirming the expression of β-synth nucleoproteins in glutamate energy synapses.
a total of 393 patients with cerebrospinal fluid β-synth nucleoprotein.
According to the diagnosis, there are 7 groups: AD, behavioral variant frontal lobe dementia (bvFTD), synactal nucleopathy (Parkinson's disease (PD), Louis dementia (DLB), Parkinson's disease dementia (PDD), kerat disease (CJD), amyotrophic lateral sclerosis (ALS), disease control group (DiCon) and non-neurodegenerative control group (Con).
151 AD patients and analyzed 46 patients with cocytocyte disease diagnosed by motion disorder specialists.
all 23 CJD patients were confirmed neuropathological cases analyzed in the infectious spongior encephalopathy unit of the G?ttingen Neurology Unit.
29 ALS patients were diagnosed with explicit or possible ALS according to the revised El Escorial standard.
the Con group from Ulem included clinical and imaging manifestations of non-neurodegenerative degenerative control groups without neurodegenerative changes.
these patients receive lumbar puncture to eliminate acute inflammation of the central nervous system (facial nerve paralysis (n=26), fortrial neuropathy (n=8), tension headache (n=8), artery arteritis (n=5), Multiple neuropathy (n-4) and one of each diagnosis: sensory abnormalities, C8 syndrome, migraines, Tolusa-Hunt syndrome, Meige syndrome, pain disorder, panic disorder, post-traumatic stress disorder, sensory decline.
The DiCon group from Mannheim and Hamburg included depressive disorder (n=30), vascular dementia (n=13), subjective cognitive reporting (n=10), psychosis (n=4), paranoia (n=2), DLB (n=2), poisoning (n=2) and one in each diagnosis: Korsakow syndrome, persistent somatic pain form disorder and sedative drug dependence.
lumbar punctures are mainly performed between 13:00 and 16:00.
sample of centrifugal cerebrospinal fluid at 500 g and to equally liquid within 30 minutes and freeze at .80 degrees C.
use the commercially available ELISA kit (Fujirebio, Hanover, Germany) to quantify total cerebrospinal fluid tau (t-tau), phosphate tau (p-tau), and A beta 42.
the levels of cerebrospinal fluid and synth nucleoproteins β using the new sandwich ELISA method.
to determine batch and inter-batch repetition by analyzing three cerebrospinal fluid samples from four different trials.
ranged from 10 to 1000 pg/mL for applications with these applications.
samples that are measured again with a higher dilution than the quantitative upper limit.
sample is lower than LLOQ.
samples were stable after 5 freeze-thaw cycles and at least 2 hours at room temperature (RT) before treatment.
19 brain samples collected at Ulm University were confirmed by autopsy AD and control cases.
control group included 7 cases of non-neurodegenerative degeneration and 5 cases of ALS.
AD patients completed Braak 2-4.
the β-synthesized nucleoprotein levels measured by the newly established enzyme-linked immunosorption test (ELISA) were highly corred with antibody-free quantitative mass spectrometrography data (r=0.92 (95% CI:0.89-0.94), p<0.0001).
of cerebrospinal fluid β-synth nucleoproteins increased in patients with mild cognitive impairment (p-lt;0.0001), dementia (p-lt;0.0001), while cerebrospinal fluid β β-synapses in patients with bvFTD, Parkinson's syndrome, and ALS did not.
addition, β-synth nucleoproteins are positioned as VGLUT1-positive glutamate-energy synapses, which significantly reduce expression in brain tissue in AD patients .
this paper, a sensitive and reliable ELISA method for detecting brain-β-synthesic nucleoproteins has been successfully established.
confirmed previous mass spectrometrography observations of elevated levels of β-synth nucleoproteins in cerebrospinal fluids in AD and CJD patients, supporting their potential use as a marker of synth degenerative variants.
Halbgebauer S, Oeckl P, Steinacker P, et al in cerebrospinal fluid as an early diagnostic marker of Alzheimer's disease Journal of Neurology, Neurosurgery and Psypsy Published Online First: 30 December 2020. doi: 10.1136/jnnp-2020-324306Med Sci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Mets Medicine" or "Source: MedSci Originals" are owned by Mets Medicine and are not reproduced by any media, website or individual without authorization, and are authorized to be reproduced with the words "Source: Mets Medicine".
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