Structural Scaffolds as Anti- Alzheimer Agents.
Bhawana Sati1, Tyagi Alka1, Anurag Chaudhary2
1Department of Pharmacy, Dr. Bhawana Sati , Banasthali Vidyapith , Rajasthan, India.
Medicinal Chemistry (Shariqah (United Arab Emirates))
|August 31, 2022
Summary
Researchers are exploring novel pharmacophoric combinations to combat Alzheimer's disease (AD). This study reviews potential multi-target agents that interfere with neurotransmitter systems and protein accumulation, offering new leads for AD drug discovery.
Area of Science:
- Neuroscience
- Pharmacology
- Drug Discovery
Background:
- Alzheimer's disease (AD) dementia presents complex cognitive and behavioral challenges.
- Key characteristics of AD include neurotransmitter system dysfunction and abnormal protein accumulation.
- Novel anti-Alzheimer agents are actively being sought, with some pharmacophoric groups showing neuroprotective potential.
Purpose of the Study:
- To compile recent target/target combinations and pharmacophoric combinations for Alzheimer's disease treatment.
- To identify pharmacophoric elements that can modulate enzymatic and receptor systems.
- To explore neuroprotective agents as potential leads for multi-target drug discovery in AD.
Main Methods:
- Literature review and compilation of existing research on Alzheimer's disease targets.
- Analysis of pharmacophoric elements and their interactions with biological systems.
- Focus on multi-target strategies for drug development.
Main Results:
- Anticholinesterase drugs are currently considered a primary treatment.
- Dysfunction in serotonergic, GABAergic, noradrenergic, dopaminergic, and glutamatergic pathways are linked to AD-related alterations.
- Pharmacophoric elements show promise in interfering with these pathways.
Conclusions:
- Further study of pharmacophoric groups and their targets is crucial for developing new anti-Alzheimer drugs.
- Identifying promising therapeutic lead compounds requires understanding receptor/enzymatic systems and related hypotheses.
- Future research aims to enhance the understanding and treatment of Alzheimer's disease.
Related Concept Videos
Alzheimer's Disease: Overview
650
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
650
Alzheimer's Disease: Treatment
250
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
250
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
197
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
197
Amyloid Fibrils
9.7K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
9.7K


