Alzheimer's Disease (AD)
Alzheimer's disease (AD) is marked by the accumulation of amyloid-beta plaques, neurofibrillary tangles, and synaptic loss which results in cognitive decline and dementia. With our thorough understanding in AD therapy development, Protheragen can offer services and complete guidance to help you take your AD therapy research to market.
Overview of Alzheimer's Disease (AD)
Alzheimer's disease (AD) is the leading neurodegenerative disorder, making up about 60 to 70 percent of dementia cases across the globe. It is characterized by a gradual decline in cognitive ability, loss of memories, and changes in behavior, culminating in complete loss of functional ability. While Alzheimer's disease affects primarily those over 65 years of age, there is an early-onset variant AD which occurs before 65 and accounts for around five percent of cases.
Fig.1 Alzheimer’s disease (AD) and its pathogenesis. (Faiyaz M, et al., 2021)
Pathogenesis of Alzheimer's Disease (AD)
The underlying causes of Alzheimer’s disease (AD) include the formation of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs), along with neuroinflammation and synaptic gap injury. Disruption of Aβ plaque formation occurs through the abnormal cleavage of an amyloid precursor protein (APP) through β- and γ-secretases, resulting in toxic Aβ42 oligomers which disrupt neuronal cell signaling. NFTs result from the hyperphosphorylation of tau proteins that destabilize microtubules and impair axonal transport. Genetic factors like the APOE-ε4 genotype and mutations in PSEN1/2 accelerate these processes. Microglial activation coupled with cytokine release also burdens neurodegenerative changes through neuroinflammation.
Fig.2 Pathogenesis of Alzheimer’s disease (AD) and Parkinson’s disease (PD). (Keighron C N, et al., 2023)
Therapeutic Development for Alzheimer's Disease (AD)
| Drug Names | Mechanism of Action | Targets | NCT Number | Research Phase |
| Recombinant human serum albumin (rHSA) | Stabilizes Aβ monomers, prevents aggregation into toxic oligomers | Amyloid-beta (Aβ) | NCT06489015 | Phase I/II |
| Memantine | Non-competitive NMDA receptor antagonist; reduces glutamate excitotoxicity | NMDA receptors | NCT02553928 | Approved |
| ABBV-916 | Monoclonal antibody targeting aggregated Aβ plaques | Amyloid-beta (Aβ) | NCT05291234 | Phase II |
| Lecanemab | IgG1 monoclonal antibody binding Aβ protofibrils and plaques | Soluble Aβ oligomers & fibrils | NCT03887455 | Approved |
Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.
Our Services
Protheragen offers modern diagnostic and therapeutic development services for rare neurodegenerative diseases such as Alzheimer's disease (AD). We seek to advance AD pathology understanding by constructing sophisticated disease models, employing novel blood-brain barrier (BBB) models to improve the delivery of therapeutics. We endeavor to construct precise diagnostic tools and potent therapeutics for AD by employing a holistic approach.
Therapeutic Development Services
By Molecule Types
At Protheragen, we address the challenges encountered in Alzheimer's disease (AD) drug development by utilizing our extensive multimodal platforms which accelerate therapeutics from discovery to clinical translation.
By Mechanism of Action
Protheragen is focused on formulating bespoke neurotherapeutic drugs which target the disease-causing processes of Alzheimer's disease (AD) for innovative forms of treatment.
Disease Model Development Services
In Vitro Model Development
- APP/PS1 Transgenic Model
- 5xFAD Transgenic Model
- APP Knock-in Model
- Tau Knock-in Model
- TREM2 Knockout Model
- Other Models
Focusing on preclinical research, Protheragen offers comprehensive pharmacodynamic (PD), pharmacokinetic (PK), and toxicology study services to support the development and regulatory approval of potential therapies. If you are interested in our services, please feel free to contact usfor more details and quotation information of related services.
References
- Faiyaz M, Ganayee M A, Akhtar S, et al. Nanomaterials in Alzheimer's disease treatment: a comprehensive review[J]. Frontiers in Bioscience-Landmark, 2021, 26(10): 851-865.
- Keighron C N, Avazzadeh S, Goljanek-Whysall K, et al. Extracellular vesicles, cell-penetrating peptides and miRNAs as future novel therapeutic interventions for Parkinson’s and Alzheimer’s disease[J]. Biomedicines, 2023, 11(3): 728.