English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

A growing body of evidence suggests that Alzheimer's disease (AD) is a multifactorial disease resulting in the well-known, common neuropathological pathway characterized by extracellular fibrillar β amyloid (Aβ) deposits in the brain, intracellular neurofibrillary tangles (NFT) and neuronal as well as axonal degeneration. While fairly accurate, the clinical diagnosis of probable AD based on standard diagnostic criteria does not take into account the long preclinical and prodromal course of AD. AD-related pathophysiological changes can occur many years and even decades before the appearance of clinical dementia syndrome. Biomarkers that are related to the pathophysiology of AD may thus help detect the preclinical stages of disease, and improve early and differential diagnosis. Here, we provide an overview of current literature on the core AD biomarkers, Aβ and phosphor-tau (p-tau), on different methods and modalities of assessing them [e.g., cerebrospinal fluid (CSF) analysis and PET imaging], and on their diagnostic and predictive value in preclinical and clinical stages of AD.

Amyloid β (Aβ) and phospho-tau (p-tau) as diagnostic biomarkers in Alzheimer's disease