Alzheimer´s Disease and Symptomatic Relief Drugs

Alzheimer´s Disease and Symptomatic Relief Drugs

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The cognition-enhancing effects of a particular drug may offer only symptomatic relief against AD. These effects need to be considered separately from other possible neuroprotective/neurorestorative effects. Compounds that exhibit the latter characteristics are designed to alter the progression and course of the disease by improving brain function by facilitating recovery or preventing neuronal cell loss. A notable example is P7C3, a 5-HT6 receptor agonist, has been shown to promote neurogenesis within a couple of days in mice models. Theoretically, the neuroprotective benefits of this compound would be able to promote neuronal genesis in human models as well. Other serotonin receptors influence memory in different ways for instance, the 5-HT4 receptors has a possible link in influencing the regulation of non-amyloidogenic soluble amyloid-beta precursor protein (sAPP) and also plays a role in modifying acetylcholine transmission.(10 on reference page on google docs).
The significance of serotonergic receptor modulation in a clinical setting remains controversial. Most of the evidence which supports this theory comes from data gathered in pre-clinical models. Many of the ligands that have been recently developed are still in the preliminary phases of testing. Another argument for the benefits of targeting the serotonergic system comes from clinical evidence. Some unconventional antipsychotic drugs that affect the serotonergic system, has been shown to increase and improve cognition in patients with schizophrenia. (11 on reference page on google docs) With all these factors in mind, these studies and findings point to potential therapies that may arise from a better understanding of the serotonergic system and cognition.

Pathology of AD

Alzheimer’s Disease is a neurodegenerative disorder that becomes progressively worse over time. One of the major symptoms of AD is the increasing inability of patients to process short-term memory efficaciously and an inability to consolidate and acquire new memories. The inability to form new memories extends to all of the senses and includes the difficulty to recall any recently observed or learned facts. As the disease progresses, caretakers are eventually required as the patients become more dependent on them for normal functioning, and this dependency eventually reaches a state where the patient is unable to effectively take care of themselves. The biggest risk factor for AD is age and most of the observed cases are people who are aged 65 years or older. The chance of getting Alzheimer’s increases significantly as a person ages, and a higher incidence of Alzheimer’s is reported in elderly patients.

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Genetics has been observed to play a role as a risk factor of AD. People who carry the apolipoprotein E4 (ApoE4) have a significantly higher chance of having late-onset AD and impaired cognition. As many as 80% of clinically identified subjects between the ages of 65 to 75 carry at least one copy of the E4 allele. (12 on google docs) Carriers of the ApoeE4 allele (Caucasian, Japanese) have a 10 to 30 fold increased risk of developing AD ages 70-80 than their peers who do not carry any E4 alleles. A proposed mechanism is that people with the E4 allele have a compromised ability to break down the Abeta plaques in the brain, which leads to excessive amyloid buildup in the brain that is one of the physiological markers of AD. Currently, there are no disease-modifying therapies available and treatment of the disease is only capable of slowing down the progression of the disease. Certain pharmacological agents have been observed to have positive benefits in combating AD, but the mechanisms of how they do so and the benefits of these mechanisms is largely unknown.
Two major theories have gained a lot of traction in the scientific community as potential reasons to why there is an associated memory loss in AD patients. These two hypotheses, either working in tandem or by themselves, (i) cholinergic and (ii) amyloid will be discussed in the following section briefly.

2.1 Cholinergic Hypothesis
The cholinergic hypothesis is mainly based on the significant loss of cholinergic neurons observed in patients suffering from AD, especially in the basal forebrain. There is more neuronal loss seen in the cerebral cortex and other areas, leading to less cholinergic neurotransmission which contributes significantly to the deterioration of cognitive function in patients. (13) There is support for this claim, because when patients are given a drug that increase acetylcholine (the main neurotransmitter for cholinergic neurons), memory has been shown to improve. (14) Currently there are a few drug options that are used extensively to manage the cognitive deficiencies for patients suffering from mild to moderate AD. These drugs include donepezil (RS)-2-[(1-benzyl- 4-piperidyl)methyl]-5,6-dimethoxy-2,3-dihydroinden- 1-one] and tacrine (1,2,3,4-tetra- hydroacridin-9-amine). These therapeutic drugs are typically acetylcholinesterase inhibitors (AChE), and work by preventing the breakdown and metabolism of synaptic acetylcholine. The increase of available acetylcholine in the synapse seems to compensate for the loss of cholinergic neurons, although the benefits of this particular method are observed for only just a few years within the disease progression timeline. Neuronal cell loss eventually occurs and if there is no action taken against that, then the drugs become less effective as there are fewer synapses remaining.

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