Critical Review Alzheimer's disease

Alzheimer is the most common type of dementia caused by the degeneration of neurons that lead to the gradual deterioration of brain functions that are integral to the normal occupational and social functioning of an individual. A detailed analysis of the biological features of the disease, possible preventive, diagnostic or treatment measures, and the on-going research efforts with promising breakthroughs in dealing with the disease provides an informed standpoint on the Alzheimer Disease. Symptoms The symptoms Alzheimer’s disease correlate to cognitive dissonance and include reduced ability to process information, impaired reasoning, changes in personality and behavior, impaired speaking, reading, and writing, and impaired visuospatial abilities. Visuospatial abilities involve or rather entail the lack of recognition of familiar faces and objects used in the daily performance of various activities, alexia or difficulties in reading written messages or texts, and difficulties in making distinctions of parallel parts of a scene at once.

The outlined symptoms are also indicative of dementia but make for Alzheimer’s disease based on the longevity of their manifestation in a patient and the severity of the damage to and deterioration of the patient’s intellectual and functional abilities (Goran Šimić1, 2017). The patient may also be suffering from loss of sense of direction and initiative and experience difficulties in performing their routine activities. The third stage, Moderate AD, refers to the progressive damage of parts of the cerebral cortex that control speech, processing of senses, reasoning, and conscious thought. The symptoms, especially behavioral changes, become more pronounced and thus demanding close monitoring of the patients which could pose psychological challenges to the close family members acting as their caregivers.

The symptoms of mild cognitive impairment intensify in this stage but indicators specific to this stage include significantly short concentration spans, problematic reading, writing, and erotic arithmetic ability, difficulties in recognizing family members and friends, paranoia, loss of impulse control, and loss of basic motor skills. The severe Alzheimer disease stage is shown to involve the rapid spread of plaques and tangles all over the brain leading loss of communication ability and recognition of family members or close acquaintances is lost completely. Familial AD as it is commonly referred is linked to the inheritance of the dominant autosomal with their onset taking place earlier than the perceivably standard 65 years of a patient’s age. Occurring at an extensive interval of between 2 to 3 generations, familial AD results from the mutations of three primary genes; the amyloid precursor protein (APP), presenilin-1 (PS1) and presenilin-2 (PS2).

Mutations of APP, PS1, and PS2, on chromosomes 21, 14, and 1 respectively lead to excessive production of 42-amino acid form of peptide Ab. The 42-amino acid form of the Ab peptide presumably contain some toxic properties capable of destroying the neurons, initiate synapse loss, and the formation of lesions such as senile plaques (SPs) and Neurofibrillary tangles (NFTs). Nevertheless, the toxic-producing mutations only account for a small percentage of the early onset familial Alzheimer’s disease and thus throwing off the predominance associated with the genetic risk factors albeit its mild influence. The enzyme is postulated to achieve its impact by catalyzing the oxidative deamination of both the xenobiotic and biogenic amines of the brain. Monoamine oxidase mainly targets neurotransmitters that correlate to its substrates in within the brain and is also integral to the metabolism of the neuroactive and vasoactive amines in the central nervous system (CNS).

The enzyme affects the functions of neurotransmitters such as epinephrine (EP), dopamine (DP), and serotonin and has a modulating effect on a range of bodily functions depicted through behavioral change and other forms of dementia. Increased modulation of these functions and on the neurotransmitters by activated monoamine oxidase leads to negative behavioral change such as mood swings, anxiety, shortening of attention span, and depression which are characteristic features of AD. The theory further proves to be a more substantial biological basis as monoamine oxidase inhibitors significantly reduce the modulation of the neurotransmitters and protect the cholinergic system from destruction thus reducing the progression of AD. The Cholinesterase inhibitors (ChEIs) serve to increase the concentration of acetylcholine and prolong the acetylcholine action in synapses by protecting it from degradation from predatory enzymes.

The four inhibitors have also proved to improve cognitive functions and initiate positive behavioral changes in AD diagnosed patients. All the agents for ChEI drug therapy exhibit the same efficacy level though the benefits of the drugs depend on the severity of the behavioral and cognitive decline. Patients with mild cognitive decline may not need close supervision and hence can be given donepezil due to its simple prescription detail of a single dosage per day. • Monoamine-based treatments in Alzheimer’s disease include the use of therapeutic drugs such as the agonist prazosin and antagonist propranolol both show much hope in improving behavioral disorders such as aggression and agitation emanating from the noradrenergic system. It can also induce gastrointestinal effects for some patients thus requiring them to take it with meals.

One of the risks for high risk and exceptional treatment is that it denies the patient their autonomy as it is the practitioners who make decisions for them. It is difficult to establish whether the actions taken by the practitioners are in the best interest of the patients and often fails to honor the patient-doctor relationship. Among the benefits include the fact that the high risk treatment offers psychological support to the caregivers whose need for emotional support during their stay with a loved diagnosed with AD is often sidelined. The caregivers have a tendency of developing depressive emotional behaviors as the experience of monitoring a loved ones as the gradually lose their cognitive abilities can be so traumatizing. The region in the brain that is associated with identifying odor or smells is the same one that controls memories and hence defects in the sense of smell can also serve as indicators to cognitive decline and consequently serve in the detection of Alzheimer’s disease.