Molecular Pathomechanisms and Biomarkers of Alzheimer's Disease

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (28 June 2023) | Viewed by 2192

Special Issue Editors


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Guest Editor
Institute of Immunology, Faculty of Medicine, Comenius University in Bratislava, Odborárske nám. 14, 81108 Bratislava, Slovakia
Interests: Alzheimer's disease; autoimmunity; immunogenetics; neurodegenerative diseases; neuroinflammation; multiple sclerosis
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Institute of Immunology, Faculty of Medicine, Comenius University in Bratislava, Odborárske nám. 14, 81108 Bratislava, Slovakia
Interests: Alzheimer's disease; immunogenetics; HLA typing; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia in elderly people. With approximately 50 million cases worldwide, AD represents a major medical and socio-economic burden. The most common form of the disease is sporadic late-onset AD, which accounts for approximately 90% of all cases and typically develops after the age of 65. AD is a multifactorial disease that results from a complex interplay between environmental, lifestyle, genetic, and epigenetic factors. Despite significant advancements in recent decades, the exact cause of the disease and processes leading to the development of amyloid and tau pathology, neuroinflammation, neurodegeneration, and other AD-related abnormalities are still not fully understood. Efforts to uncover the key cellular and molecular players in the pathological process promise the establishment of new screening, diagnostic, predictive, and monitoring biomarkers for AD as well as the development of novel effective therapeutic strategies.

In this Special Issue, we aim to publish review and original research articles that could fuel the efforts to better understand the processes underlying AD development. We would like to invite submissions addressing a broad range of topics including, but not limited to, the following: genetic and epigenetic risk factors of AD, the role of innate and adaptive immune mechanisms, oxidative stress, hormones and metabolic alterations in AD development and progression, the link between the gut microbiome and AD, and new neuroimaging and biofluid-based biomarkers for AD diagnostics.

Dr. Juraj Javor
Dr. Ivana Shawkatová
Guest Editors

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Keywords

  • Alzheimer's disease
  • biomarkers, epigenetics
  • genetics
  • genomics
  • immune mediators
  • neurodegeneration
  • neuroinflammation
  • proteomics
  • transcriptomics

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Published Papers (1 paper)

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Research

17 pages, 2954 KiB  
Article
Repurposing Diltiazem for Its Neuroprotective Anti-Dementia Role against Intra-Cerebroventricular Streptozotocin-Induced Sporadic Alzheimer’s Disease-Type Rat Model
by Ramesh Alluri, Eswar Kumar Kilari, Praveen Kumar Pasala, Spandana Rajendra Kopalli and Sushruta Koppula
Life 2023, 13(8), 1688; https://doi.org/10.3390/life13081688 - 4 Aug 2023
Cited by 2 | Viewed by 1877
Abstract
Alzheimer’s disease (AD) is an age-related neuropsychiatric disorder and a common cause of progressive dementia. Diltiazem (DTZ), the non-dihydropyridine benzothiazepine class of calcium channel blocker (CCB), used clinically in angina and other cardiovascular disorders, has proven neurological benefits. In the present study, the [...] Read more.
Alzheimer’s disease (AD) is an age-related neuropsychiatric disorder and a common cause of progressive dementia. Diltiazem (DTZ), the non-dihydropyridine benzothiazepine class of calcium channel blocker (CCB), used clinically in angina and other cardiovascular disorders, has proven neurological benefits. In the present study, the neuroprotective anti-dementia effects of DTZ against intra-cerebroventricular-streptozotocin (ICV-STZ)-induced sporadic AD (SAD)-type rat model was investigated. ICV-STZ-induced cognitive impairments were measured via passive avoidance and Morris water maze tasks. Anti-oxidative enzyme status, pro-inflammatory markers, and amyloid-beta (Aβ) protein expression in rat brain tissues were measured using ELISA kits, Western blotting, and immunostaining techniques. The data revealed that ICV-STZ injection in rats significantly induced cognitive deficits and altered the levels of oxidative and pro-inflammatory markers (p < 0.05~p < 0.001). Treatment with DTZ (10 mg/kg, 20 mg/kg, and 40 mg/kg, p.o.) daily for twenty-one days, 1 h before a single ICV-STZ (3 mg/kg) injection, significantly improved cognitive impairments and ameliorated the ICV-STZ-induced altered nitrite, pro-inflammatory cytokines (TNF-α, and IL-1β) and anti-oxidative enzyme levels (superoxide dismutase, lipid peroxidation, and glutathione). Further, DTZ restored the increased Aβ protein expression in ICV-STZ-induced brain tissue. Considering the results obtained, DTZ might have a potential therapeutic role in treating and managing AD and related dementia pathologies due to its anti-dementia activity in SAD-type conditions in rats induced by ICV-STZ. Full article
(This article belongs to the Special Issue Molecular Pathomechanisms and Biomarkers of Alzheimer's Disease)
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