Alzheimer's disease (AD) is the most common cause of dementia and accounts for 60-70 % of all cases. It affects millions of people worldwide. AD poses a substantial economic burden on societies and healthcare systems. AD is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and impaired daily functioning. As the prevalence of AD continues to increase, understanding its pathogenesis, improving diagnostic methods, and developing effective therapeutics have become paramount. This comprehensive review delves into the intricate mechanisms underlying AD, explores the current state of diagnostic techniques, and examines emerging therapeutic strategies. By revealing the complexities of AD, this review aims to contribute to the growing body of knowledge surrounding this devastating disease. 

Pathogenesis, Diagnostics, and Therapeutics for Alzheimer's Disease: Breaking the Memory Barrier

The strategy for the development of new drugs for Alzheimer's disease (AD) recognizes that an effective therapy requires early therapeutic intervention and a multifactorial approach that considers the individual initiators of AD development. Current knowledge of AD includes the understanding of pathophysiology, risk factors, biomarkers, and the evolving patterns of biomarker abnormalities. This knowledge is essential in identifying potential molecular targets for new drug development. This review summarizes promising AD drug candidates, many of which are currently in phase 2 or 3 clinical trials. New agents are classified according to the Common Alzheimer's Disease Research Ontology (CADRO). The main targets of new drugs for AD are processes related to amyloid beta and tau neurotoxicity, neurotransmission, inflammation, metabolism and bioenergetics, synaptic plasticity, and oxidative stress. These interventions are aimed at preventing disease onset and slowing or eliminating disease progression. The efficacy of pharmacotherapy may be enhanced by combining these drugs with other treatments, antioxidants, and dietary supplements. Ongoing research into AD pathophysiology, risk factors, biomarkers, and the dynamics of biomarker abnormalities may contribute to the understanding of AD and offer hope for effective therapeutic strategies in the near future. 

Alzheimer's disease approaches - Focusing on pathology, biomarkers and clinical trial candidates

Therapeutic effects of telomerase-derived peptide GV1001 in experimental autoimmune encephalomyelitis: Inhibiting neuroinflammation and promoting remyelination

A neurodegenerative condition called Alzheimer's disease (AD) impairs neurocognitive function and hinders the growth of mental ability. This neuropathological condition presents with neurodegeneration, neuronal loss, and the development of neurofibrillary tangles and Ab plaques. Dementia, neuronal loss, and the development of neurofibrillary tangles and Ab plaques are the hallmarks of this neuropathological disorder. Such a medication is not able to cure Alzheimer's disease. The drug that's now available just treats symptoms. Two major obstacles to research are the blood-brain barrier, which reduces the effectiveness of treatments, and the incomplete comprehension of the ethology of Alzheimer's disease. Stem cell-based therapy has been seen as a novel, reliable and successful restoration technique to treat AD since the condition is complex and has not gotten much attention. The latest advances in nanotechnology occasionally offer proactive treatment chances that can help get over limitations. In this overview, we concentrate on the causes of AD and the various methods used to treat them. 

Alzheimer’s Disease: An Outline of Therapeutic Interventions by different Approaches

[This corrects the article on p. 41 in vol. 17, PMID: 30906391.].

Erratum: Plasma Oligomeric Beta Amyloid in Alzheimer's Disease with History of Agent Orange Exposure

IC‐P‐079: Transient Global Amnesia: Thorough Study of 183 Cases from One Center

The efficacy and safety of GV1001 have been demonstrated in patients with moderate-to-severe Alzheimer's disease (AD). In this study, we aimed to further demonstrate the effectiveness of GV1001 using subscales of the Severe Impairment Battery (SIB), which is a validated measure to assess cognitive function in patients with moderate-to-severe AD.We performed a post hoc analysis of data from a 6 month, multicenter, phase 2, randomized, double-blind, placebo-controlled trial with GV1001 (ClinicalTrials.gov, NCT03184467). Patients were randomized to receive either GV1001 or a placebo for 24 weeks. In the current study, nine subscales of SIB-social interaction, memory, orientation, language, attention, praxis, visuospatial ability, construction, and orientation to name- were compared between the treatment (GV1001 1.12 mg) and placebo groups at weeks 12 and 24. The safety endpoints for these patients were also determined based on adverse events.In addition to the considerable beneficial effect of GV1001 on the SIB total score, GV1001 1.12 mg showed the most significant effect on language function at 24 weeks compared to placebo in both the full analysis set (FAS) and per-protocol set (PPS) (p=0.017 and p=0.011, respectively). The rate of adverse events did not differ significantly between the 2 groups.Patients with moderate-to-severe AD receiving GV1001 had greater language benefits than those receiving placebo, as measured using the SIB language subscale. 

Effects of GV1001 on Language Dysfunction in Patients With Moderate-to-Severe Alzheimer’s Disease: Post Hoc Analysis of Severe Impairment Battery Subscales

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Erratum: Plasma Oligomeric Beta Amyloid in Alzheimer's Disease with History of Agent Orange Exposure

IC‐P‐079: Transient Global Amnesia: Thorough Study of 183 Cases from One Center

Effects of GV1001 on Language Dysfunction in Patients With Moderate-to-Severe Alzheimer’s Disease: Post Hoc Analysis of Severe Impairment Battery Subscales