The Latest Articles on Amyloid-β

Our staff editors continue to share exciting, interesting, and thought-provoking reading material in the recommended articles series.

This week, we would like to share several latest articles on Amyloid-β.

Title: Early detection of Alzheimer's disease by measuring amyloid β-42 concentration in human serum based on liquid crystals
Authors: Houriyeh Sohrabnavi, Mohammad Mohammadimasoudi, Hassan Hajghassem
Type: Research article
Abstract:
Amyloid beta (Aβ) protein is one of main biomarkers for the diagnosis of Alzheimer's disease (AD). The detection of Aβ in the blood leads to the identification of people prone to AD years before the appearance of the disease. Since the concentration of Aβ in the blood is very low, it is still challenging to detect Aβ using a sensitive, simple and rapid sensor. Herein, we fabricate a new type of liquid crystal-based biosensor to detect Aβ. This sensor is based on the interaction between the negative DNA aptamer and the cationic surfactant called Cetyltrimethylammonium bromide (CTAB). The response time of this setup is about a few minutes and has a good specificity for Aβ in Human Serum (HS). The specific aptamer provided high sensitivity for the sensor with a limit of detection of Aβ as low as 100 pg/ml. The fabricated sensor is inexpensive, easy manufactured and rapid. The proposed system can be a promising strategy for early diagnosis of AD and prevention of side effects of this disease. © 2017 Elsevier Inc. All rights reserved.
Access this article: https://doi.org/10.1016/j.snb.2023.134966

Title: Self-calibrating surface-enhanced Raman scattering-lateral flow immunoassay for determination of amyloid-β biomarker of Alzheimer's disease
Authors: Xinyu Liu, Xiaoming Su, Mingyang Chen, Yangcenzi Xie, Ming Li
Type: Research Article
Abstract:
Rapid early diagnosis of Alzheimer's disease (AD) is critical for its effective and prompt treatment since the clinically available treatments can only relieve the symptoms or slow the disease progression. However, it is still a grand challenge to accurately diagnose AD at its early stage because of the indiscernible early symptoms and the lack of sensitive detection tools. Here, we develop a self-calibrating surface-enhanced Raman scattering (SERS)-lateral flow immunoassay (LFIA) biosensor for quantitative analysis of amyloid-β1-42 (Aβ1-42) biomarker in biofluids, enabling accurate AD diagnosis. The designed SERS-LFIA biosensor makes full use of the unique aspects of the LFIA format and the SERS technique to quantify the Aβ1-42 level in complex biofluids with high sensitivity, excellent anti-interference capability, low-cost, and operation simplicity. The key aspect of the design of this biosensor is that internal standard (IS)-SERS nanoparticles are embedded in the test line of the test strip as a self-calibration unit for correction of fluctuations of SERS signals caused by various external factors such as test parameters and sample heterogeneity. We demonstrate significant improvement of the detection performance of the SERS-LFIA biosensor for ratiometric quantification of Aβ1-42 owing to the built-in IS in the test line. We expect that the present IS-based biosensing strategy provides a promising tool for accurate AD diagnosis and longitudinal monitoring of therapeutic response with great promises for clinical translation.
Access this article: https://doi.org/10.1016/j.bios.2023.115840

Title: The amyloid-β peptide: Guilty as charged?
Authors: M. Paul Murphy, Valeria A. Buzinova, Carrie E. Johnson
Type: Research Article
Abstract:
Recent years have seen both considerable progress and controversy in the Alzheimer's disease (AD) field. After decades of slow to negligible movement towards the development of disease modifying therapies, promising outcomes in recent clinical trials with several monoclonal antibodies targeting various forms of the amyloid-β (Aβ) peptide have at last opened a possible way forward. In fact, at this point multiple anti-Aβ therapeutics are close to receiving (or have already received) regulatory approval. Although these outcomes are not without some degree of divisiveness, the fact remains that targeting amyloid for removal has finally shown at least modest efficacy in slowing the otherwise relentless progression of the disease. Although the validation of the long standing amyloid cascade hypothesis would seem to be at hand, what remains is the puzzling issue of why – if Aβ indeed causes AD – does removing it from the brain not stop the disease entirely.
Access this article: https://doi.org/10.1016/j.bbadis.2023.166945

Title: Imaging of Amyloid-beta-related Arteritis
Authors: Aaron Bangad BA, Mehdi Abbasi MD, Sam Payabvash MD, Adam de Havenon MD, MSCI
Type: Review Article

Key points:
Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder that is characterized by the accumulation of amyloid-beta peptide (Aβ) within the brain’s leptomeninges and smaller sized blood vessels.
ABRA is a vasculitis of the central nervous system related to an inflammatory response to Aβ in the vascular walls, which necessitates differentiating ABRA from noninflammatory CAA, as ABRA may require immunosuppressive treatment.
MR imaging is the most commonly used imaging modality to identify

Summary:
Inflammation of small vessels in the brain due to immunogenicity related to amlyoid-beta vascular deposition can manifest in ABRA, CAA-RI, or ARIA. The variety of abnormal imaging findings that these conditions can lead to are detailed above, but are not entirely pathognomonic. Because the majority of patients with ABRA or CAA-RI will improve with immunosuppression,19 it is of critical importance that the vast array of potential imaging findings indicate inflammatory CAA are documented.
Access this article: https://doi.org/10.1016/j.nic.2023.09.001

Title: Effects of DHA (omega-3 fatty acid) and estradiol on amyloid β-peptide regulation in the brain
Authors: Didier Majou, Anne-Lise Dermenghem
Type: Review article
Abstract:
In the early stages of sporadic Alzheimer’s disease (SAD), there is a strong correlation between memory impairment and cortical levels of soluble amyloid-β peptide oligomers (Aβ). It has become clear that Aβ disrupt glutamatergic synaptic function, which can in turn lead to the characteristic cognitive deficits of SAD, but the actual pathways are still not well understood. This opinion article describes the pathogenic mechanisms underlying cerebral amyloidosis. These mechanisms are dependent on the amyloid precursor protein and concern the synthesis of Aβ peptides with competition between the non-amyloidogenic pathway and the amyloidogenic pathway (i.e. a competition between the ADAM10 and BACE1 enzymes), on the one hand, and the various processes of Aβ residue clearance, on the other hand. This clearance mobilizes both endopeptidases (NEP, and IDE) and removal transporters across the blood–brain barrier (LRP1, ABCB1, and RAGE). Lipidated ApoE also plays a major role in all processes. The disturbance of these pathways induces an accumulation of Aβ. The description of the mechanisms reveals two key molecules in particular: (i) free estradiol, which has genomic and non-genomic action, and (ii) free DHA as a preferential ligand of PPARα-RXRα and PPARɣ-RXRα heterodimers. DHA and free estradiol are also self-regulating, and act in synergy. When a certain level of chronic DHA and free estradiol deficiency is reached, a permanent imbalance is established in the central nervous system. The consequences of these deficits are revealed in particular by the presence of Aβ peptide deposits, as well as other markers of the etiology of SAD.
Access this article: https://doi.org/10.1016/j.brainres.2023.148681