(Help tackle the disease using the 'lock-and-key hypothesis, as they act like enzymes)
Alzheimer's occurs when levels of acetylcholine (a neurotransmitter for memory and learning) are reduced. Donepezil is an acetylcholine inhibitor that inhibits the enzyme acetylcholinesterase, which breaks down acetylcholine in the synapse. This leads to increased acetylcholine levels, temporarily improving cognitive function.
The disease also results from a high concentration of glutamate accumulated in the brain. Riluzole inhibits glutamate release from nerve terminals, blocks some postsynaptic receptors, and inhibits voltage-gated sodium channels. Riluzole protects neurons since excess glutamate causes excitotoxicity (overstimulation of neurons, particularly the neurotransmitter glutamate). It is neuroprotective, but does not reverse damage.
(Acts like antagonists, which bind with receptors and inhibit around enzymes' active sites
A vaccine bottle of the lecanemab drug
An approved type of anti-amyloid antibody, it helps to bind with soluble amyloid-β protofibrils, which are intermediate deposits formed during the aggregation of amyloid-β proteins, and are toxic aggregates believed to drive neurodegeneration. It helps clear these aggregates via the immune system activity - called microglia. It is a disease-modifying therapy, unlike symptomatic treatments like Donepezil.
As an NMDA Receptor Antagonist, Memantine reduces abnormal activity caused by glutamate overactivation. There can be an overactivation of NMDA receptors by glutamate, leading to calcium overload and neuron death. Memantine blocks these receptors selectively, preventing excitotoxicity* while preserving normal transmission.
Excitotoxicity refers to a process where neurons are damaged or killed due to excessive activation of their receptors by excitatory neurotransmitters, primarily glutamate.