Alzheimer's Disease—115 Years after Its Discovery 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2993

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Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal
Interests: diabetes; Alzheimer’s disease; mental disorders; mitochondria; oxidative stress; uncoupling proteins; brain metabolism
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Dear Colleagues,

It has been a long journey since Alois Alzheimer, a dedicated German physician, first linked Auguste Deter’s symptoms of deteriorating memory, disorientation, decreasing speech abilities, and lack of judgment to the detection of two characteristic brain lesions, neurofibrillary tangles, and extracellular deposits that were later named senile plaques—a discovery that would make his name a household term throughout the world! Now, at 115 years after this discovery, the massive international research effort has contributed to uncovering several pieces of key information about the causes and accelerators of the development of Alzheimer’s disease (AD) and its progression. From the amyloid cascade, tau aggregation, inflammation and the immune system, cholinergic hypothesis, vascular alterations, and estrogen alterations to oxidative stress, mitochondrial dysfunction, hypometabolism, insulin resistance, gut dysbiosis, etc., many have been the theories and approaches used to tackle one of science’s most difficult puzzles. And, despite previous failures impeding advancement toward effective treatments, current investigations of new medications, non-pharmacological interventions as well as the development of biomarkers and diagnostic tests to monitor disease presence and progression offer the hope of discovering an opportunity—or window—for preventing or arresting AD progression. In this Commemorative Special Issue, we intend to present an overview of the state-of-the-art of this interesting story including the important recent advances and the latest research and milestones in AD research. For this Special Issue, we welcome the submission of original high-quality research and review articles focused on (i) diagnostic tools; (ii) in vivo and in vitro models of the disease; (iii) molecular mechanisms underlying the onset and progression of the disease; and (iv) therapeutic strategies aimed to counteract the advances of AD.

Dr. Susana Cardoso
Dr. Cristina Carvalho
Dr. Sónia Catarina Correia
Guest Editors

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  • diagnostics tools
  • therapeutics
  • Alzheimer’s disease
  • AD hypotheses
  • AD models

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Published Papers (1 paper)

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37 pages, 1157 KiB  
Current Advances in Mitochondrial Targeted Interventions in Alzheimer’s Disease
by Tiago Sousa, Paula I. Moreira and Susana Cardoso
Biomedicines 2023, 11(9), 2331; - 22 Aug 2023
Cited by 5 | Viewed by 2513
Alzheimer’s disease is the most prevalent neurodegenerative disorder and affects the lives not only of those who are diagnosed but also of their caregivers. Despite the enormous social, economic and political burden, AD remains a disease without an effective treatment and with several [...] Read more.
Alzheimer’s disease is the most prevalent neurodegenerative disorder and affects the lives not only of those who are diagnosed but also of their caregivers. Despite the enormous social, economic and political burden, AD remains a disease without an effective treatment and with several failed attempts to modify the disease course. The fact that AD clinical diagnosis is most often performed at a stage at which the underlying pathological events are in an advanced and conceivably irremediable state strongly hampers treatment attempts. This raises the awareness of the need to identify and characterize the early brain changes in AD, in order to identify possible novel therapeutic targets to circumvent AD’s cascade of events. One of the most auspicious targets is mitochondria, powerful organelles found in nearly all cells of the body. A vast body of literature has shown that mitochondria from AD patients and model organisms of the disease differ from their non-AD counterparts. In view of this evidence, preserving and/or restoring mitochondria’s health and function can represent the primary means to achieve advances to tackle AD. In this review, we will briefly assess and summarize the previous and latest evidence of mitochondria dysfunction in AD. A particular focus will be given to the recent updates and advances in the strategy options aimed to target faulty mitochondria in AD. Full article
(This article belongs to the Special Issue Alzheimer's Disease—115 Years after Its Discovery 2.0)
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