RECENT ADVANCES IN UNDERSTANDING AND MANAGING ALZHEIMER'S DISEASE: FROM PATHOGENESIS TO TREATMENT

Objective: The objective of this article is to conduct a comprehensive review of recent advances in understanding the pathogenesis of Alzheimer's disease (AD) and innovations in its management, emphasizing how these developments can inform more effective therapeutic strategies. Initially, this study explores contemporary findings related to the molecular and cellular mechanisms contributing to AD pathology, including the aggregation of beta-amyloid and tau, neural inflammation, synaptic dysfunction, as well as the impact of genetic and environmental factors. Theoretical Framework: Alzheimer's disease (AD) presents itself as a growing challenge for global public health, given its rising prevalence and the significant impact on the affected individuals, their families, and the healthcare systems. Method: A systematic review was conducted using major scientific databases to collect relevant articles on recent advances in the understanding and management of Alzheimer's disease, from pathogenesis to treatment. Specific keywords were used to identify studies addressing new findings and interdisciplinary therapeutic strategies. This enabled the synthesis of effective approaches and the identification of research gaps, supporting evidence-based clinical practices. Results and Discussion: Recent research has identified novel genetic markers linked to Alzheimer's disease, enhancing early diagnosis. Studies have also demonstrated the efficacy of integrated cognitive therapies in slowing disease progression. Additionally, new pharmacological treatments targeting amyloid plaques have shown promise in clinical trials. However, challenges in uniform treatment efficacy across diverse populations highlight the need for tailored therapeutic approaches.


INTRODUCTION
Alzheimer's disease (AD) is the leading cause of dementia and is rapidly becoming one of the most expensive, deadly, and burdensome diseases of this century.Since 2016, significant developments have occurred in understanding the underlying pathology, recognizing multiple causative and protective genes, identifying new blood and imaging biomarkers, and the first cautious signs of positive effects from disease-modifying treatments and lifestyle interventions (Scheltens et al., 2016;Scheltens et al., 2021).In 2018, Alzheimer's Disease International (ADI) estimated that approximately 50 million people around the world were suffering from dementia, with projections indicating that this number could triple by the year 2050.Notably, two-thirds of these individuals reside in low-and middle-income countries, highlighting an uneven distribution of the dementia burden that challenges the health systems of these nations.This projection underscores the urgent need for public health policies and interventions tailored to the socioeconomic realities of these countries to address the growing impact of dementia globally (ADI, 2018).
The original description of the pathology by Alois Alzheimer in the early 20th century focused on characteristic neuropathology, which includes senile plaques and neurofibrillary tangles.However, it was only in the 1980s that the neuropathological definition was refined, including the identification of comorbid neuropathologies (Lopez;González;Léger, 2019).
These conditions often coexist and significantly contribute to the clinical dementia picture observed in patients, complicating diagnosis and disease management (Khan;Barve;Kumar, 2020).The most significant risk factors for Alzheimer's disease include advanced age, generally defined as over 65 years, although this age limit is not absolutely fixed, reflecting variability in the disease's manifestation.Additionally, the presence of at least one ε4 allele of the APOE gene emerges as a predominant genetic indicator.This allele is associated with an increased risk of developing the disease, underscoring the importance of genetic predispositions in the panorama of risk factors for Alzheimer's disease.This combination of age and genetic factors highlights the complexity and multifactorial nature of the disease's pathogenesis, requiring a holistic and individualized approach to prevention and clinical management ( Van et al., 2018).
The clinical diagnostic criteria for Alzheimer's disease have undergone significant evolution, encompassing not only the symptomatic phase but also the recognition of pre-clinical stages of the disease.Recently, criteria using biomarkers to identify these early, often asymptomatic stages have been developed, enabling earlier interventions.This innovation is crucial, as it allows for diagnosis before the development of significant clinical symptoms, opening new perspectives for treatment and understanding of disease progression (Khan;Barve;Kumar, 2020;Scheltens et al., 2021).
Alzheimer's disease is currently recognized as the most prevalent form of neurodegenerative dementia.Beyond its vast impact on society at large, this disease presents a disproportionate burden on minority populations, exacerbating existing inequalities in terms of access to healthcare, diagnostic resources, and treatment opportunities (Khan;Barve;Kumar, 2020).This uneven distribution of the disease burden requires special attention in the development of public health strategies that are inclusive and equitable.Therefore, advances in diagnostic criteria and a deeper understanding of the neuropathology of Alzheimer's disease are crucial.They not only improve our ability to detect and treat the disease in its early stages but also contribute to a better understanding of the underlying mechanisms that can lead to more effective interventions.This evolution in the field of neurology promises not only to improve clinical outcomes for patients but also to offer insights into how interventions can be tailored to address the needs of vulnerable and under-represented populations ( Van et al., 2018;Khan;Barve;Kumar, 2020;Scheltens et al., 2021).Despite these advances, there are still significant barriers to effective AD treatment, mainly due to the complexity of the disease and individual variability in treatment response.
Therefore, it is crucial to continue exploring diversified and personalized therapeutic strategies, based on genetics, lifestyle, and specific clinical characteristics of patients.With this, the aim of this article is to present a comprehensive review of recent advances in understanding and managing Alzheimer's disease, from investigating its pathogenesis to developing new treatment strategies.We seek to synthesize innovations in diagnosis, discuss emerging therapies, and reflect on the challenges and future opportunities in the field, aiming to improve clinical outcomes and the quality of life of individuals affected by this debilitating condition.

METHODOLOGY
This study represents a systematic review of the literature, focused on exploring recent advances and emerging strategies in the treatment and understanding of Alzheimer's disease.
The aim of this review is to consolidate existing knowledge on the pathogenic foundations, clinical consequences, and new therapeutic approaches, identify gaps in the literature, and offer a comprehensive overview that can assist healthcare professionals and researchers in developing future interventions.Initially, a systematic search was conducted in major scientific databases, including PubMed, Scopus, Web of Science, as well as Google Scholar, using keywords such as "Alzheimer's disease", "therapeutic strategies for Alzheimer's", "Alzheimer's prevention", and "advances in Alzheimer's treatment".The inclusion criteria covered articles published in English and Portuguese that described recent developments in understanding and treating Alzheimer's disease, including studies on pharmacological therapies, neurological interventions, and cognitive management methods.Data analysis was conducted through a narrative approach, organizing the information into four main categories: efficacy of new therapies, innovative treatment methods, strategies for sustained prevention of disease progression, and the impact of these advances on the quality of life of patients.This structuring allows not only a deep understanding of the critical and innovative aspects in Alzheimer's research but also assesses the promising effects and potential adversities of these interventions on the well-being of individuals.This method of systematic review and subsequent narrative synthesis aims to provide detailed and up-to-date information on the advances in understanding and treatment of Alzheimer's disease, serving as a valuable resource for enhancing clinical 6 practices and therapeutic strategies in addressing this complex neurodegenerative condition.

ALZHEIMER'S DISEASE
Alzheimer's disease (AD), recognized as one of the main causes of dementia, is characterized as a progressive neurodegenerative disease that leads to a continuous decline in cognitive functions.Dementia, in its clinical spectrum, includes symptoms such as memory loss, thinking difficulties, language impairment, and reduced problem-solving abilities.These clinical manifestations significantly impair the autonomy and quality of life of the individuals affected.According to the World Health Organization's (WHO) update on the epidemiology of AD in 2013, the global scenario is alarming, with predictions that the number of people suffering from dementia will triple by the year 2050.In 2010, the estimate was approximately 35.6 million individuals affected by dementia worldwide, highlighting the urgency for effective public health measures and advances in research to tackle this growing epidemic.This anticipated increase underscores the critical need for developing preventive strategies, early diagnoses, and more effective treatments to mitigate the devastating impact of AD and improve care and support for patients and their families (Khan;Barve;Kumar, 2020).
The initial stage of Alzheimer's disease, referred to as the cellular phase, develops concurrently with the accumulation of β-amyloid, which triggers the spread of the pathology associated with tau protein.The predisposition to Alzheimer's disease shows a 60-80% dependence on hereditary factors, with over 40 genetic risk loci already identified; among these, the APOE gene alleles exhibit the most significant correlation with the pathology.Studies have shown that the presence of the APOE ε4 allele, in particular, is strongly associated with an increased risk of developing the disease, suggesting a crucial role in its etiology (Scheltens et al., 2021).There are various mechanisms involved in Alzheimer's disease, such as Aβ plaqueassociated neurodegeneration, neurofibrillary degeneration, synaptic dysfunction, neurotransmitter imbalance, and neuroinflammation, among others (Khan;Barve;Kumar, 2020).
According to the amyloid hypothesis, β-amyloid (Aβ) plaques form and deposit in different regions of the brain, being recognized as foreign material, which triggers an inflammatory and immune response.This involves the activation of microglia and the release of cytokines, resulting in cell death and neurodegeneration.Aβ plaques are composed of Aβ and causing neuronal death.However, there is controversy over this hypothesis, as drugs that inhibit the formation of amyloid plaques have not proven effective in reversing or halting cognitive decline, suggesting that the focus should be on therapeutic interventions that act on other targets, such as tau proteins, inflammation, and oxidative stress (Grimm, 2012;Barage;Sonawane, 2015;Begcevic et al., 2018;Mullane;Williams, 2018).
Neurofibrillary degeneration is also related to tau proteins, which are neuronal proteins associated with microtubules.Tau proteins have a microtubule-binding domain, crucial for the polymerization and stabilization of microtubules, thus maintaining the integrity of the cytoskeleton.This binding is regulated by the phosphorylation of serine/threonine residues by various kinases, such as Fyn kinase, glycogen synthase kinase-3β (GSK3β), and cyclindependent kinase 5 (CDK5).CDK5 plays a significant role in the formation of neurofibrillary tangles.Beta-amyloid (Aβ) activates calpain and deregulates p35, an activator of CDK5.Due to excess cytosolic calcium, p35 is cleaved into p25, which hyperactivates CDK5, resulting in the hyperphosphorylation of tau proteins.Hyperphosphorylation decreases the affinity of tau proteins for microtubules, leading to the formation of neurofibrillary tangles (NFTs) that deposit in the cytosol and lose the ability to maintain cellular structure.This deposition affects normal cellular functions, such as synaptic transmission, axonal transport, and signal transduction, culminating in the gradual degeneration of the cell.The main reason for hyperphosphorylation is attributed to mutations in the tau protein genes or the dysregulation of kinases and phosphatases that catalyze the phosphorylation process (Crews;Masliah, 2010;Huang et al., 2019;Khan;Barve;Kumar, 2020).
The cholinergic system plays a crucial role in the cognition process, and its dysfunction is associated with various forms of dementia, including Alzheimer's disease (AD).The cholinergic neurons of the basal nucleus of Meynert are particularly vulnerable, exhibiting deposition of amyloid plaques and neurofibrillary tangles (NFTs), which eventually leads to neuronal degeneration.This process is exacerbated by pro-inflammatory events, resulting in further cognitive deterioration.The cholinergic deficit also compromises the permeability of 8 the blood-brain barrier, causing inadequate transport of metabolites and hindering the removal of amyloid plaques, worsening the disease's progression.Alterations in the Ca2+-permeable nacetylcholine receptor (nAChR) may compromise synaptic integrity.Additionally, serotonin is also involved in the pathogenesis of AD, evidenced by the loss of serotonergic neurons in the brainstem and the reduction of this neurotransmitter's levels in many AD patients.The loss of inhibitory control of GABAergic neurons over cholinergic and glutamatergic neurons is associated with the synaptic injury observed in these patients.Therefore, the complex interaction of various neurotransmitters is essential to maintain intact cognition, and the imbalance of any of them can contribute to the deterioration of AD symptoms (Grimm;Hatmann, 2012;Hampel et al., 2018;Leanza;Gulino;Zorec, 2018;Khan;Barve;Kumar, 2020).
Neuroinflammation plays a central role in the pathogenesis of Alzheimer's disease (AD).
Although acute inflammation serves a protective function by defending the brain against injuries such as the presence of β-amyloid (Aβ) plaques, persistent activation of microglia results in an inability to remove these plaques while the release of pro-inflammatory cytokines continues.This leads to an imbalance between pro-inflammatory and anti-inflammatory cytokines, exacerbating neuronal degeneration.In addition to microglia, other cells such as endothelial cells, oligodendrocytes, and neurons can also contribute to neuroinflammation.
Various molecules with protective functions against inflammation are present in neurons, including fractalkine, complement defense proteins CD59 and CD200.Furthermore, immunological molecules such as IL-1β, IL-6, and CCL2 are produced by cerebral endothelial cells in response to Aβ plaques, perpetuating the inflammatory cycle and contributing to the progression of AD (Heppner;Ransohoff;Becher, 2015;Khan;Barve;Kumar, 2020).
In the study conducted by Khan, Barve, and Kumar (2020), the authors highlight a series of additional mechanisms involved in the pathogenesis of Alzheimer's disease, beyond the already known processes.They emphasize that infectious diseases can play a significant role in the progression of AD, triggering systemic and cerebral inflammatory responses that exacerbate neurodegeneration.The disruption of the gut microbiome, which regulates the immune system and maintains neural homeostasis, is also mentioned, with intestinal dysbiosis directly influencing neurodegenerative processes via the gut-brain axis.Genetic mutations in genes such as APP, PSEN1, PSEN2, and the APOE ε4 allele are pointed out as critical risk factors, promoting the abnormal production of Aβ peptides and the formation of amyloid plaques.
Oxidative stress, characterized by an imbalance between the production of free radicals and the body's antioxidant capacity, results in oxidative damage to proteins, lipids, and DNA, contributing to cellular dysfunction and death.Moreover, dysfunction of autophagy, a vital process for the degradation and recycling of damaged cellular components, results in the accumulation of misfolded proteins and protein aggregates, exacerbating the pathology of AD.
These mechanisms, such as infectious diseases, disruption of the gut microbiome, genetic mutations, oxidative stress, and autophagy dysfunction, highlight the complexity of AD and the need for multifaceted therapeutic approaches to effectively combat this devastating neurodegenerative condition.
Currently, the diagnosis of Alzheimer's disease (AD) primarily relies on positron emission tomography (PET) with tracer molecules and the analysis of proteins in cerebrospinal fluid (CSF).Phosphorylated tau 181 (P-tau181) serves as a confirmatory and prognostic biomarker, being deposited in the brain and secreted into the CSF, which crosses the bloodbrain barrier and enters the bloodstream, enabling its use as a diagnostic marker.Recently, diagnostic accuracy has significantly improved with specialized PET, showing 100% specificity and 96% sensitivity, even in patients with mild symptoms.PET ligands such as florbetapir, florbetaben, and flutemetamol are used, although their high cost limits widespread adoption.CSF analysis for p-tau, Aβ42, and total tau protein is a less expensive alternative, with an accuracy of 85-90%, but it is invasive and time-consuming due to the need for lumbar puncture and the limited availability of specialized laboratories.Both PET and CSF analysis demonstrate high precision, and the choice of the ideal method depends on factors such as patient and provider preference, cost, and availability.Both methods reveal that pathological changes in AD begin two decades before clinical symptoms, suggesting that diagnosis at the onset of symptoms already coincides with advanced stages of cognitive impairment, making early detection crucial (Weller;Budson, 2018;Bateman et al., 2012;Bateman;Barthélemy;Horie, 2020;Janelidze et al., 2020;Thijssen et al., 2020;Khan;Barve;Kumar, 2020).
With this, it is imperative that research continues to focus on less invasive and more accessible diagnostic methods, as well as therapies that may delay or halt disease progression.
The importance of scientific advances cannot be underestimated, as they not only improve the quality of life for patients but also offer hope for future interventions that could significantly alter the course of AD.Continued innovation and discovery are crucial to developing more effective treatments and, eventually, finding a cure for this devastating neurodegenerative condition.Association.These initiatives integrated the use of biomarkers, allowing for a classification of Alzheimer's disease based on biological foundations, marking a significant transition in how the disease is identified and categorized (McKhann et al., 1984;Dubois et al., 2007;Dubois et al., 2010;McKhann et al., 2011;Knopman;Petersen;Jack, 2019;Scheltens et al., 2021).
Initially, the diagnosis of Alzheimer's disease was confined to the stage of dementia, characterized as a clinical syndrome that manifests through progressive and profound cognitive impairment, affecting multiple functional domains.This stage also includes neurobehavioral symptoms of sufficient severity to have a significant functional impact on the daily lives of patients.A person with dementia experiences a significant loss of independence, which is the main feature distinguishing dementia from milder forms of cognitive impairment.In this context, while mild cognitive impairment may still allow a certain degree of autonomy and functionality, dementia implies substantial dependence on daily activities and care, reflecting a more marked deterioration of mental and physical capabilities (Jack et al., 2018;Scheltens et al., 2021).
Furthermore, ongoing research into the mechanisms by which β-amyloid and tau interact and accumulate is providing new insights into the early processes of neurodegeneration in Alzheimer's disease.Understanding how these proteins affect neuronal function is crucial for identifying steps that lead to cognitive impairment and cell death.These advances reveal the complexity of interactions between β-amyloid and tau, elucidating altered signaling pathways, such as mitochondrial dysfunction, oxidative stress, and neuroinflammation.Therapies that reduce β-amyloid load or prevent tau hyperphosphorylation have shown potential in preliminary clinical trials.Additionally, biomarkers such as phosphorylated tau and Aβ42 peptide in cerebrospinal fluid, along with brain imaging techniques, have revolutionized early diagnosis of the disease.These advancements enable early interventions, improving prognoses and the quality of life of patients, and alleviating the burden on health systems and families.Therefore, continued investment in research is essential for finding a definitive cure (Scheltens et al., 2021).
Recently, new biomarkers have emerged, including PET imaging techniques and plasma analyses of β-amyloid and phosphorylated tau, which demonstrate substantial potential for both clinical applications and scientific research.Additionally, preventive trials based on multidomain lifestyle approaches have indicated cognitive benefits for individuals at high risk of developing dementia.Although lifestyle factors do not directly interfere with the pathology of Alzheimer's disease, they can still positively influence outcomes in affected patients.
A biomarker is a crucial indicator for assessing normal biological and pathological processes, as well as the pharmacological effects of any therapy.In the context of Alzheimer's disease (AD), biomarkers are used to assess the overall health and condition of elderly patients.
The two main pathological features of AD are the extracellular deposition of β-amyloid (Aβ) protein and the aggregated form of hyperphosphorylated tau protein in the brain.Recently, Lashley et al. (2018) critically discussed all the important molecular biomarkers of AD, assessing their current state and future prospects.These biomarkers are fundamental for early diagnosis, monitoring disease progression, and evaluating the efficacy of therapeutic interventions, contributing to better clinical management and the development of more effective treatment strategies (Strimbu;Tavel, 2010;Humbel, 2011;Hansson et al., 2018;Lashley et al., 2018;Khan;Barve;Kumar, 2020).
Early detection of Alzheimer's disease (AD) has become a priority in the field of neurology, as it allows for more effective interventions and improves clinical outcomes for patients.One of the new strategies for early detection of AD is the advanced use of biomarkers.
Biomarkers present in cerebrospinal fluid (CSF), such as phosphorylated tau (p-tau) and betaamyloid peptide (Aβ42), are indicative of early pathological changes in the brain, long before the manifestation of clinical symptoms.CSF analysis, despite being invasive, provides a direct measure of these proteins and, when combined with brain imaging techniques, offers a more accurate and earlier diagnosis of AD.Furthermore, blood and urine biomarkers, such as lipid biomarkers, are being investigated as less invasive alternatives for the early detection of AD (Björkhem;Meaney, 2004;Schupf et al., 2008;Cermenati et al., 2015;Yang et al., 2018;Blennow;Zetterberg, 2018;Khan;Barve;Kumar, 2020).for identifying individuals at risk of developing AD (Poirier et al., 1993;Harold et al., 2009;Begcevic et al., 2018;Khan;Barve;Kumar, 2020).
Genomics and proteomics are also playing a crucial role in the early detection of Alzheimer's disease (AD).Genetic sequencing can identify mutations in genes associated with an increased risk of the disease, such as the apolipoprotein E (APOE ε4) gene.Protein biomarkers in the blood, such as Brain-Derived Neurotrophic Factor (BDNF) and the Kidney/Brain protein (KIBRA), which is associated with memory, are being investigated for their potential to indicate early changes related to AD.Additionally, proteomic analysis of blood samples and other body fluids can reveal protein expression patterns that indicate the onset of AD pathology, allowing for the identification of individuals at risk before symptoms appear (McEvoy et al., 2009;Porter et al., 2018;Khan;Barve;Kumar, 2020).
Finally, emerging technologies such as artificial intelligence (AI) and machine learning are revolutionizing the early detection of AD.Advanced algorithms are capable of analyzing large volumes of clinical, genetic, and imaging data to identify subtle patterns that may be precursors to the disease.These tools can help clinicians make more accurate and faster diagnoses, as well as customize treatment strategies for each patient based on their specific profile.The integration of these technologies with traditional clinical practices promises a more hopeful future in managing Alzheimer's disease, with earlier diagnoses and more effective treatments (Johnson et al., 2012;Fantoni et al., 2018;Khan;Barve;Kumar, 2020).

RESULTS AND DISCUSSIONS
Alzheimer's disease remains one of the greatest challenges for medicine and public health worldwide.The complexity of its pathogenesis and the variability in symptom manifestation make the task of developing effective diagnostics and treatments a pressing Furthermore, the integration of artificial intelligence and machine learning in diagnostic and treatment processes is transforming the clinical management of Alzheimer's disease.These technologies allow for deeper and more detailed analysis of large volumes of data, facilitating the identification of patterns that precede clinical symptoms and enhancing the efficacy of therapeutic interventions.This innovative approach not only increases the efficiency of treatments but also personalizes patient care, enhancing the likelihood of better clinical outcomes and reducing the emotional and financial burden on patients and their families.Therefore, it is imperative that ongoing research and development in neurology and related technologies be supported and expanded.Continued collaboration between researchers, clinicians, and industries is crucial to capitalize on these advances and translate them into tangible benefits for patients with Alzheimer's disease.With the sustained commitment of the scientific community and adequate support from public policies and private investments, the future of Alzheimer's disease management looks promising, offering hope for a significant impact on the quality of life of these patients and potentially paving the way for a cure.
___________________________________________________________________________ Rev. Gest.Soc.Ambient.| Miami | v.18.n.1 | p.1-17 | e07461 | 2024.10 3.2 RECENT ADVANCES The diagnosis of Alzheimer's disease has evolved significantly since the time of Alois Alzheimer (1864-1915), moving from a strictly pathological approach to a clinical and exclusionary method established in 1984.This initial clinical diagnosis was based on criteria defined by the National Institute of Neurological Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association, employing a combined approach of clinical and biological criteria.This model was later refined by the International Working Group, with ongoing efforts from the National Institute on Aging and the working groups of the Alzheimer's In addition to traditional biomarkers, brain imaging techniques have significantly advanced.Specialized positron emission tomography (PET) allows for the visualization of β-amyloid plaques and tau neurofibrillary tangles directly in the brain.Recently, new PET ligands, such as florbetapir, florbetaben, and flutemetamol, have been developed to enhance the specificity and sensitivity of the diagnosis.These imaging techniques are essential not only for early diagnosis but also for monitoring disease progression and the efficacy of therapeutic interventions over time.Furthermore, markers of mild cognitive impairment (MCI) are crucial

5 CONCLUSION
priority.Recently, significant advances have been made in understanding the molecular and cellular mechanisms underlying the disease.Detailed studies on the interaction and accumulation of β-amyloid and tau have provided new insights into the early processes of neurodegeneration, establishing a solid foundation for more targeted and effective interventions.The evolution in the use of biomarkers has been particularly transformative.Biomarkers in cerebrospinal fluid (CSF), such as phosphorylated tau and β-amyloid, along with blood and urinary biomarkers, are enabling more accurate and earlier diagnoses.The integration of these biomarkers with advanced brain imaging techniques, such as positron emission tomography (PET), has significantly improved the ability to detect pathological changes before the onset of clinical symptoms.This capability for early diagnosis is crucial for implementing therapeutic interventions at early stages, potentially slowing the progression of the disease.In addition to diagnostic methods, therapeutic innovations have shown considerable promise.Therapies aimed at reducing β-amyloid load or preventing tau hyperphosphorylation are in advanced stages of development and clinical trials.Genetic and proteomic research is identifying new therapeutic targets and helping to customize treatments based on each patient's genetic and biomolecular profile.The inclusion of markers of mild cognitive impairment (MCI) also allows for identifying individuals at risk and initiating interventions before the disease progresses to more severe stages.Emerging technology, including artificial intelligence (AI) and machine learning, is revolutionizing both the diagnosis and treatment of Alzheimer's disease.Advanced algorithms can analyze vast amounts of clinical and genetic data to identify subtle patterns associated with the onset of the disease, allowing for faster and more accurate diagnoses.These technologies are also facilitating the creation of personalized treatment strategies, tailoring interventions to the specific needs of each patient and optimizing clinical outcomes.In conclusion, recent advances in understanding and managing Alzheimer's disease represent significant progress in the fight against this devastating condition.The continuation of research and innovation is essential to transform these advances into effective clinical practices.Collaboration among researchers, healthcare professionals, and the pharmaceutical industry is crucial for developing new therapies and significantly improving the quality of life for patients.While the challenges are significant, the future of Alzheimer's disease research looks promising, bringing hope for earlier diagnoses, more effective treatments, and, eventually, a cure.___________________________________________________________________________ Rev. Gest.Soc.Ambient.| Miami | v.18.n.1 | p.1-17 | e07461 | 2024.14 In conclusion, recent advances in understanding Alzheimer's disease have been pivotal for developing more accurate diagnostics and innovative therapeutic interventions.The application of biomarkers, alongside emerging imaging and genetic technologies, promises an era of early diagnoses, enabling interventions at an early stage of the disease, which could significantly slow its progression.These developments not only improve diagnostic accuracy but also pave the way for personalized treatments, tailored to the specific biological characteristics of each patient.