Special Issue "New Trends in Alzheimer's Disease Research: From Molecular Mechanisms to Therapeutics"
Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 14164
Interests: pharmacogenomics; pharmacoepigenetics; genomics of brain disorders; neuroepigenetics; CNS drug development; neurodegenerative disorders; Alzheimer’s disease; Parkinson’s disease
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Special Issue in International Journal of Molecular Sciences: New Trends in Alzheimer’s Disease Research: From Molecular Mechanisms to Therapeutics 2.0
Alzheimer's disease (AD) is a health priority in developed societies, along with cardiovascular disease, cancer, stroke and major neuropsychiatric pathologies. The direct and indirect costs for the management of AD create a large economic burden for families, nations and health resources. The cost of worldwide dementia treatment currently exceeds USD 800 billion dollars (>1% of GDP). The average cost per patient/year ranges from USD 30,000 to USD 60,000, depending on stage of the disease, quality of medical care, social status and country. In terms of global costs (direct, indirect and social costs + costs of informal care), in 2019, the World Health Organization (WHO) estimated the total global societal cost of dementia 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 of dementia (>70%) in patients older than 75 years of age, are common presentations of dementia following frequent AD. AD is more frequent in women than in men; the prevalence of dementia is 30.5/1,000 in males and 48.2/1,000 in females.
The phenotype of AD is the consequence of the premature death of neurons associated with genomic, epigenomic, cerebrovascular and environmental factors. The clinical manifestation of dementia is characterized by progressive cognitive deterioration, behavioral changes and functional decline.
Conventionally, two forms of AD are differentiated: an early form (early onset AD, EOAD, <65 years) and a 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, which attribute the false phenotypic profile of sporadic AD to the disease.
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), formed by the hyperphosphorylation of tau proteins in microtubules and neurofilaments, likely exerting synergistic effects on AD pathogenesis. 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 daily medical care are facing important challenges regarding the management of dementia. The primary causes of AD and its pathogenic mechanisms are still unclear. Reliable biomarkers for an early diagnosis are not yet available. New drugs and novel therapeutic strategies that are able to slow down or halt the course of the disease are an urgent need, assuming that present medications are inefficient and not cost-effective. Since the disease destroys the neurons of susceptible patients for decades before showing symptoms, the golden dream of AD scientific research would be to find a preventive remedy, administered in pre-symptomatic phases, and capable of stopping the progressive destruction of the brain that leads to AD.
The objective of this Special Issue of IJMS is to offer the scientific community an open space to present new findings to (i) better understand the pathogenic mechanisms responsible for this neurodegenerative disease, (ii) identify potential predictive biomarkers that anticipate risk factors and can prophylactically intervene, and (iii) develop new preventive strategies and new forms of therapeutic intervention that slow down the course of the disease once symptoms appear. The best case scenario would be to prevent the disease from manifesting itself in those cases for which it is feasible to presymptomatically identify the risk.
Prof. Dr. Ramón Cacabelos
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- Alzheimer’s disease
- pathogenic mechanisms