Specific protein biomarker patterns for Alzheimer’s disease: improved diagnostics in progress

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Abstract

<p class="first" id="Par1">This short review looks at Alzheimer’s disease (AD) diagnosis through my own point of view, going from imaging through cerebrospinal fluid to blood proteins. Over the last couple of years, we have published two papers targeted at Alzheimer’s diagnosis. In one paper, we took an approach of selecting a specific target, namely, activity-dependent neuroprotective protein (ADNP), and our results tightened the association of ADNP blood expression with intelligence. In another paper, we took an unbiased approach of analysis of all genes expressed in lymphoblastoid cells lines and discovered changes in expression of the regulator of G-protein signaling 2 (RGS2) as a potential AD predictor. This review will assess our data in comparison to selected independent studies focusing on blood protein biomarkers as well as assessing saliva and urine samples with potential predictive value for AD. Furthermore, the review will provide directions for a combination of innovative markers, stratifying the population toward disease prevention and personalized medicine. </p>

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Most cited references 34

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Altered lysosomal proteins in neural-derived plasma exosomes in preclinical Alzheimer disease.

Edward J Goetzl, Adam L Boxer, Janice B Schwartz … (2015)

Diverse autolysosomal proteins were quantified in neurally derived blood exosomes from patients with Alzheimer disease (AD) and controls to investigate disordered neuronal autophagy.

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Autophagy has a key role in the pathophysiology of schizophrenia

A Merenlender-Wagner, A Malishkevich, Z Shemer … (2013)

Autophagy is a process preserving the balance between synthesis, degradation and recycling of cellular components and is therefore essential for neuronal survival and function. Several key proteins govern the autophagy pathway including beclin1 and microtubule associated protein 1 light chain 3 (LC3). Here, we show a brain-specific reduction in beclin1 expression in postmortem hippocampus of schizophrenia patients, not detected in peripheral lymphocytes. This is in contrast with activity-dependent neuroprotective protein (ADNP) and ADNP2, which we have previously found to be deregulated in postmortem hippocampal samples from schizophrenia patients, but that now showed a significantly increased expression in lymphocytes from related patients, similar to increases in the anti-apoptotic, beclin1-interacting, Bcl2. The increase in ADNP was associated with the initial stages of the disease, possibly reflecting a compensatory effect. The increase in ADNP2 might be a consequence of neuroleptic treatment, as seen in rats subjected to clozapine treatment. ADNP haploinsufficiency in mice, which results in age-related neuronal death, cognitive and social dysfunction, exhibited reduced hippocampal beclin1 and increased Bcl2 expression (mimicking schizophrenia and normal human aging). At the protein level, ADNP co-immunoprecipitated with LC3B suggesting a direct association with the autophagy process and paving the path to novel targets for drug design.

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18F-AV-1451 positron emission tomography in Alzheimer’s disease and progressive supranuclear palsy

Luca Passamonti, Patricia Vázquez Rodríguez, Young T. Hong … (2017)

The extent to which the tau tracer [18F]AV-1451 can differentiate between tauopathies is unknown. By comparing patients with Alzheimer’s disease and progressive supranuclear palsy (PSP), Passamonti et al. show that [18F]AV-1451 displays greater specificity for Alzheimer-related tau pathology than PSP-related pathology. A machine learning algorithm correctly diagnosed 94% of cases.