peer response – psychopathophamacology

post 1
Discuss the three stages of Alzheimer’s disease; make sure to include neurodegeneration in your discussion.
Alzheimers disease is a neurologic disorder that causes the brain to shrink (atrophy) and brain cells to die. It is the most common cause of dementia, which is characterized by a continuous decline in thinking, behavioral and social skills that affects a persons ability to function independently (Lane et al., 2018). Approximately 5.8 million people in the United States age 65 and older live with Alzheimers (DeTure et al, 2019). Out of the approximately 50 million people with dementia worldwide, between 60% and 70% are estimated to have Alzheimers disease (DeTure et al., 2019). There is a current hypothesis for Alzheimers disease. This hypothesis suggests that the formation of toxic amyloid plaques from peptides contribute to Alzheimers disease (Stahl,2013). This means that too much formation of amyloid-forming peptides or little removal of them can cause Alzheimers disease (Stahl, 2013). There is also a proposal that there are some neuron abnormalities in patients who have Alzheimers disease (Stahl, 2013). There are three stages of Alzheimers disease. These are the first stage, second stage, and third stage.
The first stage of Alzheimers disease is also known as the early stage. It is also considered to be trial or preclinical. This is characterized by asymptomatic amyloidosis. At this stage, amyloid plaques begin to build up in the brain, but people are mostly asymptomatic (Lane et al., 2018). As time progresses, they build up more in the brain and triggers neurodegeneration. It is however not clear whether the amyloid plaque causes the neurodegeneration, or it is occurring simultaneously with the disease. Even though this stage is considered silent, there is progressive accumulation of AB peptides in the brain and there is less elimination of these peptides. Further studies propose that, gray matter atrophy is linked to the release of AB peptides (Lane et al., 2018). In the first stage of Alzheimers disease, a person may function independently. He or she may still drive and do most activities. However, the individual may have memory lapses such as forgetting location od everyday objects. The induvial may also have difficulties which include coming up with the right word or name, experiencing increased trouble with planning or organizing, and losing or misplacing a valuable object. Some practices may help in slowing the progression include healthy diet, and adequate sleep.
In the second stage have mild cognitive impairment but have not developed dementia yet. Only a few people with MCI have amyloidosis that can be measured. It is however assumed that patients with MCI have progressed beyond the preclinical stage without any brain damage. Atrophy of the hippocampus is also noticed in patients with MCI. There is ventricular enlargement of about 2.5 cm cubic yearly in patients with MCI (Stahl, 2013). There is elevated cerebrospinal fluid (CSF) and this thought to be associated with neuronal loss in the brain of Alzheimers disease patients. The brain cortex also thins out which is indicative of loss of brain substance in the cortex. During this stage, the individual may have difficulty remembering events or personal history or experiencing confusion about where they are or what day it is.
The third and final stage is dementia. Individuals develop cognitive or behavioral problems that interfere with function at work or in everyday activities. With this stage, the person has amyloidosis with the neurodegeneration experienced in 1st and 2nd stages plus there is cognitive decline (Stahl, 2013). At this stage, the individual requires around the clock assistance with daily personal care. They lose awareness of their recent experiences as well as of their surroundings and they have difficulty communicating too. The individual may not be able to initiate engagement as much during this stage, but they can benefit from interaction in many ways.
post 2
Discuss the sleep wake cycle and histamines role in it?
There are several anatomical regions that are responsible for the sleep wake cycle, and I will list their roles briefly in this discussion board. The basal forebrain has various inputs from the hypothalamus and brain stem, the basal forebrain promotes cortical activity through the cholinergic neurotransmission that occurs during the wake and REM sleep. The basal forebrain participates in the sleep and wake cycle due to the neurotransmitters involved, such as glutamate, vesicular glutamate transporter, and lastly GABA (gamma-aminobutyric acid) (FALUPPECURARIU1 et al., 2020). The hypothalamus is the main sleep center, neuropeptides secreted in the hypothalamus glutamate and acetylcholine, as well as hypocretins (orexins) in the lateral hypothalamus are responsible for wakefulness. This is a lot of information, but it is important to understand the sleep wake cycle. The factors that help promote sleep are prostaglandin D2, adenosine, melatonin, serotonin, L-tryptophan, GABA, and growth factors (Huether & McCance, 2017). The reticular activating system is a bundle of nerves that helps regulates the state of consciousness by producing fast-firing brain waves that help contribute to alertness and attentiveness. During the sleep-wake transition the firing of those neurons will go at a slower rate and during the non-rem of sleep there are a high voltage of brain waves that are firing (Scammel et a., 2019).
There are two significant stages of sleep that you go into: non-Rem sleep (NREM) accounts for 75% to 80% of the sleep time and the REM (rapid eye movement) sleep is initiated 1-2 hours after non-REM sleep begins. Non-REM sleep is initiated in the thalamocortical network, and the pontine reticular formation is responsible for generating REM sleep. Non-REM sleep is further divided into 3 different phases (N1, N2, and N3) which goes from light to deep sleep (Huether & McCance, 2017). During the REM cycle which can occur in four to six cycles a night, you will experience muscle relaxation, altered heart rate, blood pressure, loss of voluntary control of the tongue and upper pharynx, and increase in cerebral blood flow. In Non-REM sleep (NREM), the basal metabolic rate falls, the temperature decreases, the heart rate, respiration, blood pressure, and muscle tone decreases. There is release of growth hormone but corticosteroids and catecholamines are depressed (Huether & McCance, 2017).
Histamines are involved in the sleep wake cycle because they are key wake supporting transmitters. According to Scammel et al., (2019), histamines are small monoamine signaling molecules in the brain the tuberomammillary nucleus (TMN) is the main neuronal source of histamines. There are four G protein coupled receptors, H1-H3 receptors are expressed through the brain. The H1 receptor is responsible for the wakeful process of histamines by depolarizing on post-synaptic neurons. The H3 is an inhibitory auto receptor cells that works by binding with histamine when it is high to reduce the activity of the cells (Scammel et al.,2019). Histamine works by using the H1 and H3 receptors to promote sleep/wake cycle. Going more in detail the TMN histamines fire faster with the levels of histamine stronger during the waking hours. During the sleeping hours histamines fire extraordinarily little during NREM and are nonexistent during REM.

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