Editorial

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Open AccessEditorial

Biochemical Biomarkers and Neurodegenerative Diseases

by Marcello Ciaccio

Brain Sci. 2021, 11(7), 940; https://doi.org/10.3390/brainsci11070940 - 16 Jul 2021

Cited by 1 | Viewed by 1839

Neurodegenerative diseases (ND) are a heterogeneous group of disorders characterized by progressive dysfunction and loss of neurons in different areas of the central nervous system or peripheral nervous system [...] Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

Research

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9 pages, 262 KiB

Open AccessArticle

FOXP3 and GATA3 Polymorphisms, Vitamin D3 and Multiple Sclerosis

by Concetta Scazzone, Luisa Agnello, Bruna Lo Sasso, Giuseppe Salemi, Caterina Maria Gambino, Paolo Ragonese, Giuseppina Candore, Anna Maria Ciaccio, Rosaria Vincenza Giglio, Giulia Bivona, Matteo Vidali and Marcello Ciaccio

Brain Sci. 2021, 11(4), 415; https://doi.org/10.3390/brainsci11040415 - 25 Mar 2021

Cited by 11 | Viewed by 2283

Abstract

Background: Regulatory T cells (Tregs) alterations have been implicated in the pathogenesis of Multiple Sclerosis (MS). Recently, a crucial role of the X-Linked Forkhead Box P3 (FoxP3) for the development and the stability of Tregs has emerged, and FOXP3 gene polymorphisms have been [...] Read more.

Background: Regulatory T cells (Tregs) alterations have been implicated in the pathogenesis of Multiple Sclerosis (MS). Recently, a crucial role of the X-Linked Forkhead Box P3 (FoxP3) for the development and the stability of Tregs has emerged, and FOXP3 gene polymorphisms have been associated with the susceptibility to autoimmune diseases. The expression of Foxp3 in Tregs is regulated by the transcription factor GATA binding-protein 3 (GATA3) and vitamin D₃. The aim of this retrospective case-control study was to investigate the potential association between FOXP3 and GATA3 genetic variants, Vitamin D₃, and MS risk. Methods: We analyzed two polymorphisms in the FOXP3 gene (rs3761547 and rs3761548) and a polymorphism in the GATA3 gene (rs3824662) in 106 MS patients and 113 healthy controls. Serum 25(OH)D3 was also measured in all participants. Results: No statistically significant genotypic and allelic differences were found in the distribution of FOXP3 rs3761547 and rs3761548, or GATA3 rs3824662 in the MS patients, compared with controls. Patients that were homozygous for rs3761547 had lower 25(OH)D3 levels. Conclusions: Our findings did not show any association among FOXP3 and GATA3 SNPs, vitamin D₃, and MS susceptibility. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

10 pages, 731 KiB

Open AccessArticle

Prognostic Role of CSF β-amyloid 1–42/1–40 Ratio in Patients Affected by Amyotrophic Lateral Sclerosis

by Tiziana Colletti, Luisa Agnello, Rossella Spataro, Lavinia Guccione, Antonietta Notaro, Bruna Lo Sasso, Valeria Blandino, Fabiola Graziano, Caterina Maria Gambino, Rosaria Vincenza Giglio, Giulia Bivona, Vincenzo La Bella, Marcello Ciaccio and Tommaso Piccoli

Brain Sci. 2021, 11(3), 302; https://doi.org/10.3390/brainsci11030302 - 27 Feb 2021

Cited by 8 | Viewed by 2596

Abstract

The involvement of β-amyloid (Aβ) in the pathogenesis of amyotrophic lateral sclerosis (ALS) has been widely discussed and its role in the disease is still a matter of debate. Aβ accumulates in the cortex and the anterior horn neurons of ALS patients and [...] Read more.

The involvement of β-amyloid (Aβ) in the pathogenesis of amyotrophic lateral sclerosis (ALS) has been widely discussed and its role in the disease is still a matter of debate. Aβ accumulates in the cortex and the anterior horn neurons of ALS patients and seems to affect their survival. To clarify the role of cerebrospinal fluid (CSF) Aβ 1–42 and Aβ 42/40 ratios as a potential prognostic biomarker for ALS, we performed a retrospective observational study on a cohort of ALS patients who underwent a lumbar puncture at the time of the diagnosis. CSF Aβ 1–40 and Aβ 1–42 ratios were detected by chemiluminescence immunoassay and their values were correlated with clinical features. We found a significant correlation of the Aβ 42/40 ratio with age at onset and Mini Mental State Examination (MMSE) scores. No significant correlation of Aβ 1–42 or Aβ 42/40 ratios to the rate of progression of the disease were found. Furthermore, when we stratified patients according to Aβ 1–42 concentration and the Aβ 42/40 ratio, we found that patients with a lower Aβ 42/40 ratio showed a shorter survival. Our results support the hypothesis that Aβ 1–42 could be involved in some pathogenic mechanism of ALS and we suggest the Aβ 42/40 ratio as a potential prognostic biomarker. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

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12 pages, 1185 KiB

Open AccessArticle

Transcranial Magnetic Resonance Imaging-Guided Focused Ultrasound with a 1.5 Tesla Scanner: A Prospective Intraindividual Comparison Study of Intraoperative Imaging

by Cesare Gagliardo, Roberto Cannella, Costanza D’Angelo, Patrizia Toia, Giuseppe Salvaggio, Paola Feraco, Maurizio Marrale, Domenico Gerardo Iacopino, Marco D’Amelio, Giuseppe La Tona, Ludovico La Grutta and Massimo Midiri

Brain Sci. 2021, 11(1), 46; https://doi.org/10.3390/brainsci11010046 - 04 Jan 2021

Cited by 3 | Viewed by 2055

Abstract

Background: High-quality intraoperative imaging is needed for optimal monitoring of patients undergoing transcranial MR-guided Focused Ultrasound (tcMRgFUS) thalamotomy. In this paper, we compare the intraoperative imaging obtained with dedicated FUS-Head coil and standard body radiofrequency coil in tcMRgFUS thalamotomy using 1.5-T MR scanner. [...] Read more.

Background: High-quality intraoperative imaging is needed for optimal monitoring of patients undergoing transcranial MR-guided Focused Ultrasound (tcMRgFUS) thalamotomy. In this paper, we compare the intraoperative imaging obtained with dedicated FUS-Head coil and standard body radiofrequency coil in tcMRgFUS thalamotomy using 1.5-T MR scanner. Methods: This prospective study included adult patients undergoing tcMRgFUS for treatment of essential tremor. Intraoperative T2-weighted FRFSE sequences were acquired after the last high-energy sonication using a dedicated two-channel FUS-Head (2ch-FUS) coil and body radiofrequency (body-RF) coil. Postoperative follow-ups were performed at 48 h using an eight-channel phased-array (8ch-HEAD) coil. Two readers independently assessed the signal-to-noise ratio (SNR) and evaluated the presence of concentric lesional zones (zone I, II and III). Intraindividual differences in SNR and lesional findings were compared using the Wilcoxon signed rank sum test and McNemar test. Results: Eight patients underwent tcMRgFUS thalamotomy. Intraoperative T2-weighted FRFSE images acquired using the 2ch-FUS coil demonstrated significantly higher SNR (R1 median SNR: 10.54; R2: 9.52) compared to the body-RF coil (R1: 2.96, p < 0.001; R2: 2.99, p < 0.001). The SNR was lower compared to the 48-h follow-up (p < 0.001 for both readers). Intraoperative zone I and zone II were more commonly visualized using the 2ch-FUS coil (R1, p = 0.031 and p = 0.008, R2, p = 0.016, p = 0.008), without significant differences with 48-h follow-up (p ≥ 0.063). The inter-reader agreement was almost perfect for both SNR (ICC: 0.85) and lesional findings (k: 0.82–0.91). Conclusions: In the study population, the dedicated 2ch-FUS coil significantly improved the SNR and visualization of lesional zones on intraoperative imaging during tcMRgFUS performed with a 1.5-T MR scanner. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

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17 pages, 3772 KiB

Open AccessArticle

Resveratrol Prevents GLUT3 Up-Regulation Induced by Middle Cerebral Artery Occlusion

by Germán Fernando Gutiérrez Aguilar, Iván Alquisiras-Burgos, Javier Franco-Pérez, Narayana Pineda-Ramírez, Alma Ortiz-Plata, Ismael Torres, José Pedraza-Chaverri and Penélope Aguilera

Brain Sci. 2020, 10(9), 651; https://doi.org/10.3390/brainsci10090651 - 20 Sep 2020

Cited by 8 | Viewed by 3111

Abstract

Glucose transporter (GLUT)3 up-regulation is an adaptive response activated to prevent cellular damage when brain metabolic energy is reduced. Resveratrol is a natural polyphenol with anti-oxidant and anti-inflammatory features that protects neurons against damage induced in cerebral ischemia. Since transcription factors sensitive to [...] Read more.

Glucose transporter (GLUT)3 up-regulation is an adaptive response activated to prevent cellular damage when brain metabolic energy is reduced. Resveratrol is a natural polyphenol with anti-oxidant and anti-inflammatory features that protects neurons against damage induced in cerebral ischemia. Since transcription factors sensitive to oxidative stress and inflammation modulate GLUT3 expression, the purpose of this work was to assess the effect of resveratrol on GLUT3 expression levels after ischemia. Male Wistar rats were subjected to 2 h of middle cerebral artery occlusion (MCAO) followed by different times of reperfusion. Resveratrol (1.9 mg/kg; i. p.) was administered at the onset of the restoration of the blood flow. Quantitative-PCR and Western blot showed that MCAO provoked a substantial increase in GLUT3 expression in the ipsilateral side to the lesion of the cerebral cortex. Immunofluorescence assays indicated that GLUT3 levels were upregulated in astrocytes. Additionally, an important increase in GLUT3 occurred in other cellular types (e.g., damaged neurons, microglia, or infiltrated macrophages). Immunodetection of the microtubule-associated protein 2 (MAP2) showed that MCAO induced severe damage to the neuronal population. However, the administration of resveratrol at the time of reperfusion resulted in injury reduction. Resveratrol also prevented the MCAO-induced increase of GLUT3 expression. In conclusion, resveratrol protects neurons from damage induced by ischemia and prevents GLUT3 upregulation in the damaged brain that might depend on AMPK activation. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

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Review

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14 pages, 1876 KiB

Open AccessReview

Imaging of Substantia Nigra in Parkinson’s Disease: A Narrative Review

by Paola Feraco, Cesare Gagliardo, Giuseppe La Tona, Eleonora Bruno, Costanza D’angelo, Maurizio Marrale, Anna Del Poggio, Maria Chiara Malaguti, Laura Geraci, Roberta Baschi, Benedetto Petralia, Massimo Midiri and Roberto Monastero

Brain Sci. 2021, 11(6), 769; https://doi.org/10.3390/brainsci11060769 - 09 Jun 2021

Cited by 10 | Viewed by 5791

Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disorder, characterized by motor and non-motor symptoms due to the degeneration of the pars compacta of the substantia nigra (SNc) with dopaminergic denervation of the striatum. Although the diagnosis of PD is principally based on a [...] Read more.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder, characterized by motor and non-motor symptoms due to the degeneration of the pars compacta of the substantia nigra (SNc) with dopaminergic denervation of the striatum. Although the diagnosis of PD is principally based on a clinical assessment, great efforts have been expended over the past two decades to evaluate reliable biomarkers for PD. Among these biomarkers, magnetic resonance imaging (MRI)-based biomarkers may play a key role. Conventional MRI sequences are considered by many in the field to have low sensitivity, while advanced pulse sequences and ultra-high-field MRI techniques have brought many advantages, particularly regarding the study of brainstem and subcortical structures. Nowadays, nigrosome imaging, neuromelanine-sensitive sequences, iron-sensitive sequences, and advanced diffusion weighted imaging techniques afford new insights to the non-invasive study of the SNc. The use of these imaging methods, alone or in combination, may also help to discriminate PD patients from control patients, in addition to discriminating atypical parkinsonian syndromes (PS). A total of 92 articles were identified from an extensive review of the literature on PubMed in order to ascertain the-state-of-the-art of MRI techniques, as applied to the study of SNc in PD patients, as well as their potential future applications as imaging biomarkers of disease. Whilst none of these MRI-imaging biomarkers could be successfully validated for routine clinical practice, in achieving high levels of accuracy and reproducibility in the diagnosis of PD, a multimodal MRI-PD protocol may assist neuroradiologists and clinicians in the early and differential diagnosis of a wide spectrum of neurodegenerative disorders. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

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19 pages, 392 KiB

Open AccessReview

Inherited Neuromuscular Disorders: Which Role for Serum Biomarkers?

by Antonino Lupica, Vincenzo Di Stefano, Andrea Gagliardo, Salvatore Iacono, Antonia Pignolo, Salvatore Ferlisi, Angelo Torrente, Sonia Pagano, Massimo Gangitano and Filippo Brighina

Brain Sci. 2021, 11(3), 398; https://doi.org/10.3390/brainsci11030398 - 21 Mar 2021

Cited by 8 | Viewed by 2696

Abstract

Inherited neuromuscular disorders (INMD) are a heterogeneous group of rare diseases that involve muscles, motor neurons, peripheral nerves or the neuromuscular junction. Several different lab abnormalities have been linked to INMD: sometimes they are typical of the disorder, but they usually appear to [...] Read more.

Inherited neuromuscular disorders (INMD) are a heterogeneous group of rare diseases that involve muscles, motor neurons, peripheral nerves or the neuromuscular junction. Several different lab abnormalities have been linked to INMD: sometimes they are typical of the disorder, but they usually appear to be less specific. Sometimes serum biomarkers can point out abnormalities in presymtomatic or otherwise asymptomatic patients (e.g., carriers). More often a biomarker of INMD is evaluated by multiple clinicians other than expert in NMD before the diagnosis, because of the multisystemic involvement in INMD. The authors performed a literature search on biomarkers in inherited neuromuscular disorders to provide a practical approach to the diagnosis and the correct management of INMD. A considerable number of biomarkers have been reported that support the diagnosis of INMD, but the role of an expert clinician is crucial. Hence, the complete knowledge of such abnormalities can accelerate the diagnostic workup supporting the referral to specialists in neuromuscular disorders. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

7 pages, 248 KiB

Open AccessReview

The Role of Vitamin D as a Biomarker in Alzheimer’s Disease

by Giulia Bivona, Bruna Lo Sasso, Caterina Maria Gambino, Rosaria Vincenza Giglio, Concetta Scazzone, Luisa Agnello and Marcello Ciaccio

Brain Sci. 2021, 11(3), 334; https://doi.org/10.3390/brainsci11030334 - 06 Mar 2021

Cited by 31 | Viewed by 3549

Abstract

Vitamin D and cognition is a popular association, which led to a remarkable body of literature data in the past 50 years. The brain can synthesize, catabolize, and receive Vitamin D, which has been proved to regulate many cellular processes in neurons and [...] Read more.

Vitamin D and cognition is a popular association, which led to a remarkable body of literature data in the past 50 years. The brain can synthesize, catabolize, and receive Vitamin D, which has been proved to regulate many cellular processes in neurons and microglia. Vitamin D helps synaptic plasticity and neurotransmission in dopaminergic neural circuits and exerts anti-inflammatory and neuroprotective activities within the brain by reducing the synthesis of pro-inflammatory cytokines and the oxidative stress load. Further, Vitamin D action in the brain has been related to the clearance of amyloid plaques, which represent a feature of Alzheimer Disease (AD), by the immune cell. Based on these considerations, many studies have investigated the role of circulating Vitamin D levels in patients affected by a cognitive decline to assess Vitamin D’s eventual role as a biomarker or a risk factor in AD. An association between low Vitamin D levels and the onset and progression of AD has been reported, and some interventional studies to evaluate the role of Vitamin D in preventing AD onset have been performed. However, many pitfalls affected the studies available, including substantial discrepancies in the methods used and the lack of standardized data. Despite many studies, it remains unclear whether Vitamin D can have a role in cognitive decline and AD. This narrative review aims to answer two key questions: whether Vitamin D can be used as a reliable tool for diagnosing, predicting prognosis and response to treatment in AD patients, and whether it is a modifiable risk factor for preventing AD onset. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

10 pages, 4152 KiB

Open AccessReview

COVID-19 and Alzheimer’s Disease

by Marcello Ciaccio, Bruna Lo Sasso, Concetta Scazzone, Caterina Maria Gambino, Anna Maria Ciaccio, Giulia Bivona, Tommaso Piccoli, Rosaria Vincenza Giglio and Luisa Agnello

Brain Sci. 2021, 11(3), 305; https://doi.org/10.3390/brainsci11030305 - 27 Feb 2021

Cited by 71 | Viewed by 8657

Abstract

The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a neurotropic virus with a high neuroinvasive potential. Indeed, more than one-third of patients develop neurological symptoms, including confusion, headache, and hypogeusia/ageusia. However, long-term neurological consequences have received little interest compared to respiratory, cardiovascular, [...] Read more.

The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a neurotropic virus with a high neuroinvasive potential. Indeed, more than one-third of patients develop neurological symptoms, including confusion, headache, and hypogeusia/ageusia. However, long-term neurological consequences have received little interest compared to respiratory, cardiovascular, and renal manifestations. Several mechanisms have been proposed to explain the potential SARS-CoV-2 neurological injury that could lead to the development of neurodegenerative diseases, including Alzheimer’s Disease (AD). A mutualistic relationship between AD and COVID-19 seems to exist. On the one hand, COVID-19 patients seem to be more prone to developing AD. On the other hand, AD patients could be more susceptible to severe COVID-19. In this review, we sought to provide an overview on the relationship between AD and COVID-19, focusing on the potential role of biomarkers, which could represent precious tool for early identification of COVID-19 patients at high risk of developing AD. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

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13 pages, 657 KiB

Open AccessReview

Arylsulfatase A (ASA) in Parkinson’s Disease: From Pathogenesis to Biomarker Potential

by Efthalia Angelopoulou, Yam Nath Paudel, Chiara Villa and Christina Piperi

Brain Sci. 2020, 10(10), 713; https://doi.org/10.3390/brainsci10100713 - 07 Oct 2020

Cited by 9 | Viewed by 3829

Abstract

Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease, is a clinically heterogeneous disorder, with obscure etiology and no disease-modifying therapy to date. Currently, there is no available biomarker for PD endophenotypes or disease progression. Accumulating evidence suggests that mutations [...] Read more.

Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease, is a clinically heterogeneous disorder, with obscure etiology and no disease-modifying therapy to date. Currently, there is no available biomarker for PD endophenotypes or disease progression. Accumulating evidence suggests that mutations in genes related to lysosomal function or lysosomal storage disorders may affect the risk of PD development, such as GBA1 gene mutations. In this context, recent studies have revealed the emerging role of arylsulfatase A (ASA), a lysosomal hydrolase encoded by the ARSA gene causing metachromatic leukodystrophy (MLD) in PD pathogenesis. In particular, altered ASA levels have been detected during disease progression, and reduced enzymatic activity of ASA has been associated with an atypical PD clinical phenotype, including early cognitive impairment and essential-like tremor. Clinical evidence further reveals that specific ARSA gene variants may act as genetic modifiers in PD. Recent in vitro and in vivo studies indicate that ASA may function as a molecular chaperone interacting with α-synuclein (SNCA) in the cytoplasm, preventing its aggregation, secretion and cell-to-cell propagation. In this review, we summarize the results of recent preclinical and clinical studies on the role of ASA in PD, aiming to shed more light on the potential implication of ASA in PD pathogenesis and highlight its biomarker potential. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

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15 pages, 848 KiB

Open AccessReview

Recent Advances on the Role of GSK3β in the Pathogenesis of Amyotrophic Lateral Sclerosis

by Hyun-Jun Choi, Sun Joo Cha, Jang-Won Lee, Hyung-Jun Kim and Kiyoung Kim

Brain Sci. 2020, 10(10), 675; https://doi.org/10.3390/brainsci10100675 - 26 Sep 2020

Cited by 23 | Viewed by 4332

Abstract

Amyotrophic lateral sclerosis (ALS) is a common neurodegenerative disease characterized by progressive motor neuron degeneration. Although several studies on genes involved in ALS have substantially expanded and improved our understanding of ALS pathogenesis, the exact molecular mechanisms underlying this disease remain poorly understood. [...] Read more.

Amyotrophic lateral sclerosis (ALS) is a common neurodegenerative disease characterized by progressive motor neuron degeneration. Although several studies on genes involved in ALS have substantially expanded and improved our understanding of ALS pathogenesis, the exact molecular mechanisms underlying this disease remain poorly understood. Glycogen synthase kinase 3 (GSK3) is a multifunctional serine/threonine-protein kinase that plays a critical role in the regulation of various cellular signaling pathways. Dysregulation of GSK3β activity in neuronal cells has been implicated in the pathogenesis of neurodegenerative diseases. Previous research indicates that GSK3β inactivation plays a neuroprotective role in ALS pathogenesis. GSK3β activity shows an increase in various ALS models and patients. Furthermore, GSK3β inhibition can suppress the defective phenotypes caused by SOD, TDP-43, and FUS expression in various models. This review focuses on the most recent studies related to the therapeutic effect of GSK3β in ALS and provides an overview of how the dysfunction of GSK3β activity contributes to ALS pathogenesis. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

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10 pages, 2194 KiB

Open AccessPerspective

Might Fibroblasts from Patients with Alzheimer’s Disease Reflect the Brain Pathology? A Focus on the Increased Phosphorylation of Amyloid Precursor Protein Tyr₆₈₂ Residue

by Filomena Iannuzzi, Vincenza Frisardi, Lucio Annunziato and Carmela Matrone

Brain Sci. 2021, 11(1), 103; https://doi.org/10.3390/brainsci11010103 - 14 Jan 2021

Cited by 7 | Viewed by 2403 | Correction

Abstract

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder with no cure and no effective diagnostic criteria. The greatest challenge in effectively treating AD is identifying biomarkers specific for each patient when neurodegenerative processes have not yet begun, an outcome that would allow the [...] Read more.

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder with no cure and no effective diagnostic criteria. The greatest challenge in effectively treating AD is identifying biomarkers specific for each patient when neurodegenerative processes have not yet begun, an outcome that would allow the design of a personalised therapeutic approach for each patient and the monitoring of the therapeutic response during the treatment. We found that the excessive phosphorylation of the amyloid precursor protein (APP) Tyr₆₈₂ residue on the APP ₆₈₂YENPTY₆₈₇ motif precedes amyloid β accumulation and leads to neuronal degeneration in AD neurons. We proved that Fyn tyrosine kinase elicits APP phosphorylation on Tyr₆₈₂ residue, and we reported increased levels of APP Tyr₆₈₂ and Fyn overactivation in AD neurons. Here, we want to contemplate the possibility of using fibroblasts as tools to assess APP Tyr₆₈₂ phosphorylation in AD patients, thus making the changes in APP Tyr₆₈₂ phosphorylation levels a potential diagnostic strategy to detect early pathological alterations present in the peripheral cells of AD patients’ AD brains. Full article

(This article belongs to the Special Issue Biochemical Biomarkers and Neurodegenerative Diseases)

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