Alzheimer's disease (AD)

Alzheimer's disease (AD) is a pr♦€÷ogressive neurodegenerative disease w± ith insidious onset. Clinically, it is ♦±&characterized by gene§₽¶ral dementia such as mem★∑€×ory impairment, aphasia, ap↕♠raxia, cognition, impairmΩγent of visual spatial skills, executiveπ  dysfunction, and per≥∏sonality and behavior changes. So f®♠ar, the cause is unknown. Currently, thβ>πe number of patients w≠↓γγith Alzheimer’s disease in China ranks ✔'βfirst in the world. And onl♥α↕y 21% of patients got staβ​¥ndardized diagnosis. →→However, the diagnosis÷₩≈♥ and treatment rate of Alzhe™™±imer’s disease is in sharp  ∞contrast to the incidence. 49% of ca ¶σses were mistaken for na ₩tural aging, and only 19♠&ε×.6% received medicati✔<←"on. The low diagnosis rate is ₹®one of the main reasons f£φ‍$or the high incidence o•±f Alzheimer's disease in my country&λ₩✔.

Biomarkers for Alzheimer's disease (AD<×✘↔)

Professor Philip Scheltens from th"↑≠e Vrije Universiteit Medicσ>al Center in Amsterdam, the Net★₩™herlands, reviewed nearly 110 years ofασ¥ research on Alzheimer’s disease ↕'(AD) biomarkers.He pointed out t→±©∏hat the diagnosis of σ↕ε∞AD has shifted from the original cli←αnical diagnosis in 19"♣ 84 to the diagnosis of objective biom>♠ ‍arkers.At the 2017AAIC con≥&✘ference, the speaker ±★✔announced in advance the 2018 NIA/AA  ♣biomarkers as the new standard for ↑∏® AD diagnosis. When the pati® ent is tested positive βφfor Aβ (A+) and Tau positive (T+), ∑≈✔$whether neurodegeneration or neuron‍↕al damage is positive (N+) or negativ₹↔↕e (N-), the patient can be clearly d‌φiagnosed as AD. AD7C-NTP, Tau-181, and •δ₽Aβ1-42 biomarkers detect ADΩ  with simple operation, strongφδ specificity and high sens↔¶‌itivity, and are suitable f★ or early census.

SPR-AD7C detection clinical δ©βapplication

AD7C-NTP is a member of the>✘ neurofilament protein fa¥∏♦¶mily. It is expressed ÷≈α♦in neurons and is located in the axo¶πns of nerve cells. Studies have shown t∞π♣hat the overexpression of the AD7c-NTP♦δ ↓ gene in the transfected ©Ω nerve cells promotes the÷← © occurrence of neuritis ∞ and cell death, And throughσ±↕↓ in situ hybridization and immunohistoδ✔γ chemical staining, it was found that t♠¥φhe increased expression of AD7c-NTP✔₩£ appeared in degenerated neurons γ★↓with intact histology.Prove tha★£₽t the expression of abnormal A≠'•D7c-NTP protein is an earl♦¥×y event of AD neurodegener≠♦<©ation, In the early stages of the​₩←₹ disease, the level of >€AD7c-NTP in the cerebrospinal flu♦££Ωid has a significant positive α≤correlation with the severity of deme•≈ ≤ntia. Therefore, AD7c-NTP is u>↔&δsed as a new molecular marker to diag★↔↓nose the elderly who have not yet devel¶ ₽<oped symptoms or have early symptomsδ&♦. Preventive treatmen≠¶‌t before the onset of symptomsλα is of great value to delay the tim'Ωe of onset.

Testing clinical app€♠★lications for SPR-Tau-181& A↕ ≥β1-42

Human phosphorylated Tau-φ¥Ω181 protein is formed by abno≥φ∑rmal hyperphosphorylati×£¥™on of tau protein in the brain. p-tau-1σγ$<81 causes abnormal entangle≈αφment of microtubule spiral fila₽​♠ments to form NFT, human β amyloi​γ♠£d 1-42 (Aβ1-42).

It is produced by the cleavage o€₩≠f brain amyloid precurs≠≥'or protein through proteol$βδ ysis. Aβ1-42 is more agg•φregating and neurotoxic♣♥₽, which promotes the form•↕ation of SP. Aβ promot•→&es the phosphorylation ♦↑of Tau protein, and Tau protein mediat& ‌es the neurotoxicity of Aβ. Aα♠β and Tau protein intera≥<↑εct with each other and promote&→¥♥ the development of AD.$λ±÷