When the name Alzheimer’s comes to thought most people associate it with senior people of old age (Toepper, 2017) . It’s mostly common among the aged, people who average 65 years and above but on other occasions, it can also manifest in younger people, a term referred to as early-onset Alzheimer’s disease. Alzheimer’s manifests itself in the form of memory loss also called dementia in better conditions (Snyder, 2015) . With time this disease worsens and expresses in the way of memory loss, losing the ability to converse and worse of it all is the loss of the ability to respond to the environmental surroundings.
Pathology of Alzheimer’s disease
It is of importance to note that in most cases AD is not primarily a disease associated with brain regions or neurotransmitter systems (Arendt, Stieler & Holzer, 2014) . Senile plaques and neurofibrillary tangles lead to loss of neurons in temporal cortex together with cholinergic neurons mostly in the nucleus of Meynert (Nuttall, Pasquini, Scherr & Sorg, 2016) . Therefore the pathology of AD is associated with neurotransmitter abnormalities.
Delegate your assignment to our experts and they will do the rest.
Firstly, Acetylcholine is also associated with is loss of cholinergic neuron; in this process, it is also important to mention that there is a decreased activity of choline acetyltransferase (Mitrasinovic & Kablar, 2017) . Hence this is what correlates to the cognitive impairment associated with AD and the consistent neuropathy findings so far. Of importance to note is that reports have shown that, estrogen can modulate and regulate the choline acetyltransferase (Au, Piers & Lancashire, 2015) . Therefore, scientists have proven that estrogen replacement can delay the manifestation of AD. Secondly, serotonin concentrations are to a greater extent decreased together with its metabolites; this is primarily in the cortical and hippocampal (Rodriguez et al., 2018) . 5HT2 serotonin gets reduced.
Besides, the concentration of dopamine gets steadily reduced, especially when one talks about the cortical and basal levels associated with ganglia (Hiroaki Tanaka, 2013) . It is also of importance to note that patients who are associated with AD may experience a disease known as Parkinson's or rather Parkinsonism, brought about by the influence of dopamine as discussed previously (Au, Piers & Lancashire, 2015) . Also, norepinephrine gets characterized by a subsequent reduction of the cortical concentration of dopamine hydroxylase and also noradrenaline. Last but not least, scientists have proved that excitatory and inhibitory amino acids glutamate and its N-methyl-D-aspartate have receptors, and these receptors have reduced concentrations, and the same can refer to the inhibitory gamma-aminobutyric acid as well as glutamic acid decarboxylase (Neuner & Kaczorowski, 2017) .
ALZHEIMER’S DIAGNOSIS AND LABORATORY FINDINGS
Alzheimer’s as we have already discussed is a dangerous disease and efforts involved in its diagnosis should be inch perfect and pinpoint. Physical tests applied to identify AD should be direct and involving and should start from the most straightforward route to the most sophisticated practices (Nuttall, Pasquini, Scherr & Sorg, 2016) . One needs to research the overall family health and the general health of the family. Trying to ask the members and close friends about the health of the individual. Look into the history in terms of behavior, eating habits and the diet, past medical incidences and the and the ability of the individual to carry out his/her activities (Linszen et al., 2018) . Also one can examine the memory stability through simple tests, checking if one can solve simple problems, if one is attentive enough and exploring how one speaks and keeps track of time (Kocahan & Doğan, 2017) .
Doctors can further carry out medical tests; in most cases, this should involve blood and urine tests. The blood test advocated for has proven its importance because it can detect a protein which identifies people with AD during the early periods of the disease — the test searches for changes especially in the levels of a neurofilament light chain (NFL) protein (Weller & Budson, 2018) . The so-called protein inhabits in the brain cells and neurons as their internal skeleton (Arendt, Stieler & Holzer, 2014) . Diagnosis of AD may also involve the use of sophisticated instruments to perform brain scans; such may include: Computer tomography, magnetic resonance imaging and even the use of positron emission tomography, this is done on most cases to rule out examples of other symptoms that may be suspect (Li, Hu, Tan, Yu & Tan, 2014) .
SIGNS AND SYMPTOMS OF ALZHEIMER’S DISEASE
Loss of memory is one of the most common manifestations of AD disease; this can get experienced during the early stages of AD (Dukart, Sambataro & Bertolino, 2015) . One forgets nearly everything even recently learned information. One tends to forget important events and keeps on asking one thing over and over again without grasping (Li, Hu, Tan, Yu & Tan, 2014) . Moreover, patients tend to have difficulties in solving simple tasks that were previously possible. Also one has problems in planning; worse still one can’t follow a daily routine or work plan and keeping track. For patients with families, they have difficulties in completing tasks in their homes, at their places of work and during their leisure activities. Some rules may prove challenging to follow.
Besides, individuals with AD disease may show signs of confusion especially when it comes to things to do with time and places they have been to before; it might shock you that they wouldn’t even remember their favorite places (Weller & Budson, 2018) . Worse still people with AD may show the poor judgment of visual images and spatial relationships. This manifests itself in the form of difficulty in reading, judging distances and also of essential to note determination of color and also contrast. Furthermore, patients with AD may have difficulty in expressing themselves and joining conversations, some may stop in the middle of a conversation, and some may go to a greater extent of even forgetting what they were talking about in the first place (Linszen et al., 2018) . Also, another sign exhibited by individuals with AD is the inability to retrace their steps and losing things. Even others misplace things entirely (Paouri & Georgopoulos, 2019) . Withdrawal from people and workplaces is another feature of this disease; it goes on further to manifest itself in the form of mood swings and personality changes which may vary in an instant.
ALZHEIMER’S DISEASE VERSUS AGE-RELATED CHANGES
Alzheimer’s if not examined well might be misinterpreted as an age-related disease which might lead to wrong diagnosis and treatment.
Table 1: Illustrates the Differences between Alzheimer’s disease and Age-Related Changes.
Alzheimer’s Disease | Age-related changes |
Poor decision-making and loss of judgment | Poor decisions made once in a while. |
Losing track of specific date completely | Forgetting a specific date can remember later |
Difficulty in conversing with others | Can have a conversation but once in a while can forget a word to use. |
Misplacing things and can’t be able to retrace back | Losing things frequently, time from time |
Withdrawn from people and social gatherings | The tendency of feeling weary most of the time especially when it involves things to do with work. |
Moods and personality tend to change. | Has developed new ways of doing things and becomes angered when disrupted. |
GENETIC COMPONENTS OF ALZHEIMER’S DISEASE
Early-Onset Alzheimer’s Disease
This has been shown to manifest itself among middle-aged individuals. Some of the significant findings show that it might be inherited (Toepper, 2017) . Parents who carry an early onset has a 50% chance of passing it to their children. Early-onset FAD arises due to several gene mutations on chromosomes 21, 14 and also 1. Mutations that occur on chromosome 21 lead to abnormal precursor protein also abbreviated as APP, on 14, it causes abnormal presenilin 1 made and on chromosome 1 leads to abnormal presenilin 2 (Karch & Goate, 2015) . These mutations play a crucial role in how APP is being broken down, and this is what leads to the formation of harmful amyloid plaques (Matsumura, 2016) .
Late-onset Alzheimer’s disease
The disease gets commonly manifested on most people of old age (Toepper, 2017) . It is said to be influenced by environmental, lifestyle and genetic factors (Karch & Goate, 2015) . The scientist has shown that having the apolipoprotein E (APOE) gene which is on chromosome 19 exposes an individual to this disease (Lambert, 2015) . APOE gets manifested in different forms which include:
APOEҽ2: is said to develop much later in life gives some protection to the condition
APOEҽ3: it is one of the most common alleles though scientist has proven its specific role, it is said d to play both roles of neither decreasing nor increasing the disease.
APOEҽ4: this increases the disease, and it leads to early manifestation of the disease.
TREATMENT AND PROGNOSIS OF ALZHEIMER’S DISEASE
Medication for memory
Cholinesterase Inhibitors are commonly used drugs and are majorly used to treat things associated with memory loss, thoughts one’s language and judgment (Xia, Jiang, McDermott & Han, 2018) . They are also used to prevent the breakdown of acetylcholine which anchors learning and memory these supporting the nerve cells (Hiroaki Tanaka, 2013) . Additionally, they are essential in terms of minimizing the symptoms and delaying the worsening of the said symptoms (Li, Hu, Tan, Yu & Tan, 2014) . Cholinesterase is mild thus easily tolerated. Secondly, Memantine is used to treat severe symptoms of the disease. It’s usually used to improve reasoning one's language and doing simple tasks. The drug is used to enhance the performance of glutamate which is typically used to process information. It also improves mental function (McCaulley & Grush, 2015) .
Creating a safe and supportive environment
Plan a way of keeping essential staffs in a place where they are easily reachable and thus are difficult to get lost. Apply and use a checklist where necessary, the medication should be kept in secure but reachable destinations (McCaulley & Grush, 2015) . Of importance to note is the reduction of the numbers of mirrors within the household, because this tends to frighten people with AD. Besides, one can go even a greater extent of removing excess furniture’s and unnecessary rags within the homestead to provide free passage (Lambert, 2015) . Last but not least, one should also avail nightlights and security objects should be paramount.
References
Arendt, T., Stieler, J., & Holzer, M. (2014). Brain hypometabolism triggers PHF-like phosphorylation of tau, a major hallmark of Alzheimer’s disease pathology. Journal Of Neural Transmission , 122 (4), 531-539. doi: 10.1007/s00702-014-1342-8
Au, R., Piers, R., & Lancashire, L. (2015). Back to the future: Alzheimer's disease heterogeneity revisited. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring , 1 (3), 368-370. doi: 10.1016/j.dadm.2015.05.006
Dukart, J., Sambataro, F., & Bertolino, A. (2015). Accurate Prediction of Conversion to Alzheimer’s Disease using Imaging, Genetic, and Neuropsychological Biomarkers. Journal Of Alzheimer's Disease , 49 (4), 1143-1159. doi: 10.3233/jad-150570
FPaouri, E., & Georgopoulos, S. (2019). Systemic and CNS inflammation crosstalk: implications for Alzheimer’s Disease. Current Alzheimer Research , 16 . doi: 10.2174/1567205016666190321154618
Hiroaki Tanaka, K. (2013). Mini Review: Pharmacotherapy for Behavioral and Psychological Symptoms in Alzheimer?s Disease. Brain Disorders & Therapy , 02 (02). doi: 10.4172/2168-975x.1000106
Karch, C., & Goate, A. (2015). Alzheimer’s Disease Risk Genes and Mechanisms of Disease Pathogenesis. Biological Psychiatry , 77 (1), 43-51. doi: 10.1016/j.biopsych.2014.05.006
Kocahan, S., & Doğan, Z. (2017). Mechanisms of Alzheimer’s Disease Pathogenesis and Prevention: The Brain, Neural Pathology, N-methyl-D-aspartate Receptors, Tau Protein, and Other Risk Factors. Clinical Psychopharmacology And Neuroscience , 15 (1), 1-8. doi: 10.9758/cpn.2017.15.1.1
Lambert, J. (2015). Genetic risk factors of Alzheimer's disease and app metabolism. Alzheimer's & Dementia , 11 (7), P163. doi: 10.1016/j.jalz.2015.07.104
Li, X., Hu, N., Tan, M., Yu, J., & Tan, L. (2014). Behavioral and Psychological Symptoms in Alzheimer’s Disease. Biomed Research International , 2014 , 1-9. doi: 10.1155/2014/927804
Linszen, M., Lemstra, A., Dauwan, M., Brouwer, R., Scheltens, P., & Sommer, I. (2018). Understanding hallucinations in probable Alzheimer's disease: Very low prevalence rates in a tertiary memory clinic. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring , 10 , 358-362. doi: 10.1016/j.dadm.2018.03.005
Matsumura, M. (2016). The Influence of Health Condition of the Caregiver: The Care Environment and the Prognosis of Patients with Alzheimer’s Disease. Alzheimer's & Dementia , 12 (7), P703. doi: 10.1016/j.jalz.2016.06.1382
McCauley, M., & Grush, K. (2015). Alzheimer’s Disease: Exploring the Role of Inflammation and Implications for Treatment. International Journal Of Alzheimer's Disease , 2015 , 1-10. doi: 10.1155/2015/515248
Mitrasinovic, O., & Kablar, N. (2017). COMPUTATIONAL APPROACHES IN PRECLINICAL DIAGNOSTICS AND PROGNOSIS FOR ALZHEIMER’S DISEASE. Alzheimer's & Dementia , 13 (7), P1005-P1006. doi: 10.1016/j.jalz.2017.06.1398
Neuner, S., & Kaczorowski, C. (2017). DISCOVERING GENETIC MODIFIERS OF ALZHEIMER’S DISEASE USING NOVEL MOUSE MODELS. Alzheimer's & Dementia , 13 (7), P975. doi: 10.1016/j.jalz.2017.06.1315
Nuttall, R., Pasquini, L., Scherr, M., & Sorg, C. (2016). Degradation in intrinsic connectivity networks across the Alzheimer's disease spectrum. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring , 5 , 35-42. doi: 10.1016/j.dadm.2016.11.006
Rodriguez, R., Molina, M., Leite, R., Sabadin, R., Takada, L., & Suemoto, C. et al. (2018). NEUROPATHOLOGICAL FINDINGS OF AN EARLY-ONSET DEMENTIA CASE WITH ATYPICAL ALZHEIMER’S DISEASE: HOW CHALLENGING CAN THE CLINICAL DIAGNOSIS OF MIXED AD BE?. Alzheimer's & Dementia , 14 (7), P432. doi: 10.1016/j.jalz.2018.06.367
Snyder, P. (2015). Introducing Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring, an open access journal of the Alzheimer's Association. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring , 1 (1), 1-4. doi: 10.1016/j.dadm.2015.01.001
Toepper, M. (2017). Dissociating Normal Aging from Alzheimer’s Disease: A View from Cognitive Neuroscience. Journal Of Alzheimer's Disease , 57 (2), 331-352. doi: 10.3233/jad-161099
Weller, J., & Budson, A. (2018). Current understanding of Alzheimer’s disease diagnosis and treatment. F1000research , 7 , 1161. doi: 10.12688/f1000research.14506.1
Xia, X., Jiang, Q., McDermott, J., & Han, J. (2018). Aging and Alzheimer’s disease: Comparison and associations from molecular to system level. Aging Cell , 17 (5), e12802. doi: 10.1111/acel.12802