New Trends in Alzheimer’s Disease Research: From Molecular Mechanisms to Therapeutics: 3rd Edition
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".
Deadline for manuscript submissions: 31 December 2025 | Viewed by 24
Special Issue Editor
Interests: pharmacogenomics; pharmacoepigenetics; genomics of brain disorders; neuroepigenetics; CNS drug development; neurodegenerative disorders; Alzheimer’s disease; Parkinson’s disease
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
This Special Issue is a continuation of “New Trends in Alzheimer’s Disease Research: From Molecular Mechanisms to Therapeutics: 2nd Edition” (https://www.mdpi.com/journal/ijms/special_issues/P73P883Z6P).
Treating Alzheimer’s disease (AD) is a priority in developed societies, along with the treatment of cardiovascular disease, cancer, stroke and major neuropsychiatric pathologies. The direct and indirect costs of AD management create a large economic burden for families, nations and healthcare systems, with the current cost of dementia treatment worldwide currently exceeding USD 800 billion (>1% of GDP). The average cost per patient/year ranges from USD 30,000 to USD 60,000, depending on the stage of the disease, quality of medical care, patient’s social status and country. In 2019, the World Health Organization (WHO) estimated the total global societal cost of dementia (direct, indirect and social costs and costs of informal care) to be about USD 1.3 trillion (>USD 2.8 trillion by 2030).
AD is the most prevalent form of dementia (50–60%). Vascular dementia (30–40%), other forms of dementia (10–15%) and mixed dementia, which is the most frequent form (>70%) in patients older than 75, are common presentations following frequent AD. AD is more frequent in women than in men, with the prevalence of dementia being 30.5/1000 in males and 48.2/1000 in females.
The phenotype of AD stems from the premature death of neurons, caused by genomic, epigenomic, cerebrovascular and environmental factors. The clinical manifestation of dementia is characterized by progressive cognitive deterioration, behavioral changes and a functional decline.
Conventionally, two forms of AD are differentiated—an early form (early-onset AD, EOAD, <65 years) and late-onset AD (LOAD, >65 years)—within an apparent pathological continuum. EOAD is associated with familial forms of Mendelian genetics (familial AD, FAD), while LOAD shows a more complex pathogenesis, in which a multitude of polymorphic variants in over 600 genes distributed throughout the human genome converge with diverse environmental factors, presenting a false phenotypic profile of sporadic AD.
Both forms of dementia exhibit common neuropathological hallmarks of amyloidopathy and tauopathy, characterized by extracellular deposits of aggregated β-amyloid (Aβ) in senile plaques and vessels (amyloid angiopathy) and intracellular neurofibrillary tangles (NFTs). These are formed by the hyperphosphorylation of tau proteins in microtubules and neurofilaments, likely exerting synergistic effects on the pathogenesis of AD. Dendritic dystrophy and desarborization, microglia activation, astrogliosis and neuronal loss are also typical neuropathological markers in the hippocampus and neocortex, where neurotransmitter deficits (cholinergic, monoaminergic, glutamatergic, GABAergic, neuropeptidergic), neurotrophic dysfunction, neuroinflammation, oxidative-stress-related lipid peroxidation and cerebrovascular (hypoperfusion) damage are also present.
The scientific community, pharmaceutical industry and healthcare system are facing important challenges regarding the management of dementia. The primary causes of AD and its pathogenic mechanisms are still unclear, and reliable biomarkers to enable early diagnosis are not yet available. Novel drugs and therapeutic strategies that are able to slow down or halt the course of the disease are urgently needed, since the present medications are inefficient and not cost-effective. Since the disease destroys susceptible patients’ neurons for decades before they show symptoms, the ultimate goal of scientific AD research would be to find a preventive remedy that could be administered in presymptomatic phases and stop the progressive destruction of the brain that leads to AD.
The objective of this Special Issue of IJMS is to offer the scientific community a space to present new findings allowing us to (i) better understand the pathogenic mechanisms responsible for this neurodegenerative disease, (ii) discover potential predictive biomarkers that can enable us to identify risk factors and prophylactically intervene, and (iii) develop new preventive strategies and forms of therapeutic intervention that slow the course of the disease once symptoms appear. The best-case scenario would be to prevent the disease manifesting in cases where it is feasible to presymptomatically identify the risk.
Prof. Dr. Ramón Cacabelos
Guest Editor
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Keywords
- Alzheimer’s disease
- pathogenic mechanisms
- genomics
- epigenetics
- biomarkers
- prevention
- treatment
- pharmacogenetics
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