Blood biomarkers: ready for clinical practice?

Coulthard, Elizabeth; Hosseini, Akram A.

doi:10.1136/jnnp-2022-330958

Cited by 2 publications

(1 citation statement)

References 13 publications

(18 reference statements)

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“…Such markers will provide the framework for patient staging and further advances in the field of pharmacotherapy [ 92 , 93 ]. In this respect, captivating findings were recently published by Altomare et al [ 94 ], who confirmed the excellent correlation, up to p < 0.001, between plasma markers and traditional scintigraphy and CSF markers. Their results showed that “overall, plasma p-tau (both alone and in combination with Aβ 42 ) showed the best performance both in terms of correlation with traditional biomarkers and of diagnostic accuracy over traditional biomarkers.” Along this line, interesting recent progress has been made by Giacomucci et al [ 95 ] on the quantitative measurement of the blood concentration of neurofilament light chain (NfL), a well-studied biomarker for AD, as an effect of treatment with hydromethylthionine mesylate (HMTM), a molecule which prevents the aggregation of tau that forms toxic fibrils causing damage to neurons.…”

Section: Discussionsupporting

confidence: 84%

Friends and Foes in Alzheimer’s Disease

Pauwels,

Boer

2023

Med Princ Pract

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Alzheimer’s disease (AD) is a disabling neurodegenerative disease. The prognosis is poor and currently there are no proven effective therapies. Most likely, the etiology is related to cerebral inflammatory processes that cause neuronal damage, resulting in dysfunction and apoptosis of nerve cells. Pathogens that evoke a neuroinflammatory response, collectively activate astrocytes and microglia, which contributes to the secretion of pro-inflammatory cytokines. This leads to the deposit of clustered fragments of beta-amyloid and misfolded tau proteins which do not elicit an adequate immune reaction. Apart from the function of astrocytes and microglia, molecular entities such as TREM2, SYK, C22 and C33 play a role in the physiopathology of AD. Furthermore, bacteria and viruses may trigger an overactive inflammatory response in the brain. Pathogens like Heliobacter pylori, Chlamydia pneumonia and Porphyromonas gingivalis (known for low-grade infection in the oral cavity) can release gingipains, which are enzymes that can damage and destroy neurons. Chronic infection with Borrelia burgdorferi (the causative agent of Lyme disease) can co-localize with tau-tangles and amyloid deposits. As for viral infections, HSV1, cytomegalovirus and Epstein-Barr virus can play a role in the pathogenesis of AD. Present investigations have resulted in the development of antibodies that can clear the brain of beta-amyloid plaques. Trials with humanized aducanumab, lecanomab and donanemab revealed limited success in AD patients. However, AD should be considered as a continuum in which the initial preclinical phase may take 10 or even 20 years. It is generally thought that this phase offers a window for efficacious treatment. Therefore, research is also focused on the identification of biomarkers for early AD detection. In this respect, the plasma measurement of neurofilament light chain in patients treated with hydromethylthionine mesylate may well open a new way to prevent the formation of tau tangles and represents the first treatment for AD at its roots.

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