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I need a rough draft by June 24th,2024 for the professor to review please.
research paper should be 5 pages MLA formated pages pages excluded images and works cited pages
One of the article used musbe be from ‘National library of medicine”  NIH .author Aditi Kumar, 
Esha Sharma ect..

Preparing the Assignment
Requirements
Read the case study below.
In your initial discussion post, answer the questions related to the case scenario and support your response with at least one evidence-based reference by Wed., 11:59 pm MT.
Provides a response using appropriate resources
Case Scenario
A 76-year -old man is brought to the primary care office by his wife with concerns about his worsening memory. He is a retired lawyer who has recently been getting lost in the neighborhood where he has lived for 35 years. He was recently found wandering and has often been brought home by neighbors. When asked about this, he becomes angry and defensive and states that he was just trying to go to the store and get some bread.
His wife expressed concerns about his ability to make decisions as she came home two days ago to find that he allowed an unknown individual into the home to convince him to buy a home security system which they already have. He has also had trouble dressing himself and balancing his checkbook. At this point, she is considering hiring a day-time caregiver help him with dressing, meals and general supervision why she is at work.
Past Medical History: Gastroesophageal reflux (treated with diet); is negative for hypertension, hyperlipidemia, stroke or head injury or depression
Allergies: No known allergies
Medications: None
Family History
Father deceased at age 78 of decline related to Alzheimer’s disease
Mother deceased at age 80 of natural causes 
No siblings
Social History
Denies smoking
Denies alcohol or recreational drug use 
Retired lawyer
Hobby: Golf at least twice a week
Review of Systems
Constitutional: Denies fatigue or insomnia
HEENT: Denies nasal congestion, rhinorrhea or sore throat.  
Chest: Denies dyspnea or coughing
Heart: Denies chest pain, chest pressure or palpitations.
Lymph: Denies lymph node swelling.
Musculoskeletal: denies falls or loss of balance; denies joint point or swelling
General Physical Exam  
Constitutional: Alert, angry but cooperative
Vital Signs: BP-128/72, T-98.6 F, P-76, RR-20
Wt. 178 lbs., Ht. 6’0″, BMI 24.1
HEENT
Head normocephalic; Pupils equal and reactive to light bilaterally; EOM’s intact
Neck/Lymph Nodes
No abnormalities noted  
Lungs 
Bilateral breath sounds clear throughout lung fields.
Heart 
S1 and S2 regular rate and rhythm, no rubs or murmurs. 
Integumentary System 
Warm, dry and intact. Nail beds pink without clubbing.  
Neurological
Deep tendon reflexes (DTRs): 2/2; muscle tone and strength 5/5; no gait abnormalities; sensation intact bilaterally; no aphasia
Diagnostics
Mini-Mental State Examination (MMSE): Baseline score 12 out of 30 (moderate dementia)
MRI: hippocampal atrophy
Based on the clinical presentation and diagnostic findings, the patient is diagnosed with Alzheimer’s type dementia.
Discussion Questions
Compare and contrast the pathophysiology between Alzheimer’s disease and frontotemporal dementia.
Identify the clinical findings from the case that supports a diagnosis of Alzheimer’s disease.  
Explain one hypothesis that explains the development of Alzheimer’s disease
Discuss the patient’s likely stage of Alzheimer’s disease.
**** my post was as follows***
“Alzheimer’s disease: Pathophysiology and diagnosis”
Question #1                  
“Alzheimer’s disease (AD)” is a neurodegenerative disorder that causes progressive cognitive decline, characterized by cholinergic dysfunction and amyloid-beta deposition. At the same time, “frontotemporal dementia (FTD)” is another type with a different pathophysiology (Yang et al., 2022). Alzheimer’s disease is one of the primary causes of dementia, accompanied by two pathological hallmarks that include amyloid-beta (Aβ) plaques and neurofibrillary tangles made up of hyperphosphorylated tau protein in the affected regions of the brain (Banchelli et al., 2021). These abnormal protein deposits impair neurons and cause their death in brain areas like the hippocampus and other cortices involved in memory, speech, and other cognitive manifestations.
“Frontotemporal dementia” is defined by the gradual demise of the frontal and temporal lobes in the brain; these are the areas involved in personality, behaviour and speech (Yang et al., 2022). It is related to aggregated and misfolded proteins, such as tau, TDP-43, or FUS, in the neurodegenerative zones mediating neuronal loss and shrinkage.
In contrast, FTD presents similarly to other cortical dementia with symptoms like social inappropriateness, personality changes, memory deficits and language disturbances, At the same time, motor features are usually less prominent until the later stages since there is no involvement of the subcortical regions, unlike in Alzheimer’s disease (Antonioni et al., 2023).
Question #2
The case presents several clinical findings that support the diagnosis of Alzheimer’s disease, including:
Declining memory function, like forgetting where one lives and getting confused, even in familiar areas like the neighbourhood.
Decision-making and judgment – he had to pay $225 to purchase an unnecessary home security system from an unrecognized man on the street.
Disabilities in carrying out activities every day on a given day, such as putting on clothes and handling money.
Yes, paternal – My father has Alzheimer’s disease (Antonioni et al., 2023).
Diagnostic findings: The vital past investigations include hippocampal atrophy on MRI and a low MMSE score of 12 out of 30, representing moderate dementia (Banchelli et al., 2021).
Question #3
Among the theories regarding the progression of Alzheimer’s disease, one of the most widely accepted is the amyloid cascade hypothesis. This hypothesis explains that “amyloid-beta (Aβ)” peptides obtained from amyloid precursor protein begin the cholesterol deposition, plaques, neurofibrillary tangles, and neuronal dysfunction and results in dementia and Alzheimer’s (Antonioni et al., 2023). This hypothesis proclaims that, due to a disruption in the equilibrium of the formation and clearance of Aβ peptides, these peptides accumulate into insoluble fibrillar structures in the brain (Yang et al., 2022). These Aβ plaques cause a cascade of events, such as the hyperphosphorylation of tau protein, forming neurofibrillary tangles, inflammation, oxidative stress, and associated neuronal death.
Based on the evidence presented, the pathogenesis process of Alzheimer’s disease cannot be solely attributed to the amyloid cascade hypothesis but somewhat could also be influenced by genetic predisposition, environmental factors and other cellular and molecular modifications. The etiology here is multifactorial, influenced by both endogenous and exogenous factors that facilitate the progression of the disease (Wareham et al., 2022). The amyloid cascade hypothesis has been embraced because of ongoing evidence supporting the theory. Still, there are some shortcomings to it, making it hard to argue that it gives all the required information about the pathogenesis of Alzheimer’s disease, which, of course,, has other sub-processes.
Question #4   
Assuming that all the information from the case scenario is accurate, the following can be said about the patient’s current state: The patient appears to be in the moderate phase of Alzheimer’s disease (Arvanitakis et al., 2019). The following findings support this assessment:
Worsening memory problems and getting lost in a familiar environment
Difficulty with decision-making and judgment, as demonstrated by the incident with the home security system
Trouble with activities of daily living, such as dressing and managing finances
A baseline MMSE score of 12/30, which falls within the range of moderate dementia (MMSE score of 10-20)
In the moderate stage of Alzheimer’s disease, individuals typically experience significant cognitive impairment, including “memory loss, difficulty with language and communication, impaired judgment and decision-making, and increasing dependence on others for daily activities”. As the disease progresses, the patient may require more assistance and supervision from caregivers.
References
Antonioni, A., Raho, E. M., Lopriore, P., Pace, A. P., Latino, R. R., Assogna, M., Mancuso, M., Gragnaniello, D., Granieri, E., Pugliatti, M., Di Lorenzo, F., & Koch, G. (2023). Frontotemporal Dementia, Where Do We Stand? A Narrative Review. International Journal of Molecular Sciences, 24(14), 11732. https://doi.org/10.3390/ijms241411732Links to an external site.
Arvanitakis, Z., Shah, R. C., & Bennett, D. A. (2019). Diagnosis and Management of Dementia: Review. Jama, 322(16), 1589–1599. https://doi.org/10.1001/jama.2019.4782Links to an external site.
Banchelli, M., Cascella, R., D’Andrea, C., La Penna, G., Li, M. S., Machetti, F., Matteini, P., & Pizzanelli, S. (2021). Probing the Structure of Toxic Amyloid-β Oligomers with Electron Spin Resonance and Molecular Modeling. ACS Chemical Neuroscience, 12(7), 1150–1161. https://doi.org/10.1021/acschemneuro.0c00714Links to an external site.
Wareham, L. K., Liddelow, S. A., Temple, S., Benowitz, L. I., Di Polo, A., Wellington, C., Goldberg, J. L., He, Z., Duan, X., Bu, G., Davis, A. A., Shekhar, K., Torre, A. L., Chan, D. C., Canto-Soler, M. V., Flanagan, J. G., Subramanian, P., Rossi, S., Brunner, T., & Bovenkamp, D. E. (2022). Solving neurodegeneration: common mechanisms and strategies for new treatments. Molecular Neurodegeneration, 17(1). https://doi.org/10.1186/s13024-022-00524-0Links to an external site.
Yang, H., Li, J., Li, X., Ma, L., Hou, M., Zhou, H., & Zhou, R. (2022). Based on molecular structures: Amyloid-β generation, clearance, toxicity and therapeutic strategies. Frontiers in Molecular Neuroscience, 15. https://doi.org/10.3389/fnmol.2022.927530Links to an external site.
post to reflect on from peer :::::::::: 
1 page in length
JADE 
Compare and contrast the pathophysiology between Alzheimer’s disease and frontotemporal dementia.
In Alzheimer’s disease (AD), there is known neuronal atrophy and a loss of synapses throughout the cerebral cortex. However, the underlying reason for why this arises is still unknown (Sheppard & Coleman, 2020). Amyloid beta plaques and neurofibrillary tau tangles have been linked to the cause of AD (Sheppard & Coleman, 2020). The inability to remove amyloid beta proteins creates toxins that later form neuritic plaques, leading to neuron death (McCance & Huether, 2019). An excess of amyloid beta protein accumulates in the smooth muscle of cerebral arteries, resulting in amyloid angiopathy and disturbed blood flow (McCance & Huether, 2019). The tau protein leads to neurofibrillary tangles, also known to result in neuron death. Both neuritis plaque and neurofibrillary tangles occur within the cerebral cortex and hippocampus, which are the brain areas essential for memory (McCance & Huether, 2019). These underlying factors known to be associated with AD and neuron death eventually cause the sulci to widen, the gyri to thin, and the ventricles to enlarge. These changes result in the symptoms seen in AD relating to memory loss since the loss of synapses prevents the workings of neurotransmitters within the brain (McCance & Huether, 2019).
Frontotemporal dementia encompasses a group of disorders characterized by the progressive loss of nerve cells in the brain’s frontal or temporal lobes, also called frontotemporal degeneration (Alzheimer’s Association, 2024). The damaged nerve cells in the frontal and temporal lobes lead to behavioral and personality changes and difficulties with language (Alzheimer’s Association, 2024). Several diseases can lead to frontotemporal degeneration, primarily those involving tau and TDP43 proteins. In frontotemporal dementia, amounts of tau and TDP43 proteins build up within the neurons of the frontal and temporal lobes, resulting in neurological changes (National Institute of Aging, 2023). These disorders preferentially target the frontal and temporal lobes, resulting in dementia, although the etiology remains unclear (Alzheimer’s Association, 2024).
Identify the clinical findings from the case that supports a diagnosis of Alzheimer’s disease.  
There are several clinical findings from this case study that support a diagnosis of AD. The most prominent symptoms supporting the patient’s AD diagnosis are those related to his current memory issues. Some risk factors for AD that the patient possesses are his age and close family history of AD. The patient’s Mini-Mental State Examination (MMSE) score of 12 out of 30 also indicates moderate dementia. Lastly, the MRI finding of hippocampal atrophy is consistent with AD.
Explain one hypothesis that explains the development of Alzheimer’s disease
The cholinergic hypothesis is one of the oldest hypotheses for AD and formed the basis for many of the drugs created for slowing AD progression (Agarwal et al., 2020). According to this theory, individuals with AD have decreased production and transportation of the neurotransmitter acetylcholine in their brains (Agarwal et al., 2020). Acetylcholine is crucial for all cholinergic nerve cells in both peripheral and central nervous systems, utilized by pre- and post-ganglionic parasympathetic and pre-ganglionic sympathetic nerve cells (Agarwal et al., 2020). Research has highlighted acetylcholine’s vital role in learning and memory. In AD, the degeneration of cholinergic neurons in the nucleus basalis of Meynert leads to the memory loss observed in patients (Agarwal et al., 2020). A significant reduction in the transcription of the enzyme choline acetyltransferase occurs in the remaining cholinergic nerve cells, resulting in decreased choline acetyltransferase activity and the onset of dementia symptoms (Agarwal et al., 2020).
Discuss the patient’s likely stage of Alzheimer’s disease.
In this scenario, the patient is likely in the middle stage of AD. The middle stage of AD is characterized by significant forgetfulness, easily getting lost, dependency on instrumental activities of daily living, and assistance with some activities of daily living (McCance & Huether, 2019). The exact symptoms will vary from patient to patient; however, in this stage, it is essential to assess and encourage the patient when it comes to the activities they are still able to perform independently (Alzheimer’s Association, 2024). As Alzheimer’s progresses throughout its middle stage, which can extend for many years, the individual will need progressively more care (Alzheimer’s Association, 2024).
References
Agarwal, M., Alam, M. R., Haider, M. K., Malik, M. Z., & Kim, D.-K. (2020). Alzheimer’s disease: An overview of major hypotheses and therapeutic options in nanotechnology. Nanomaterials, 11(1), 59-. https://doi.org/10.3390/nano11010059Links to an external site.
Alzheimer’s Association. (2024). Frontotemporal dementia. https://www.alz.org/alzheimers-dementia/what-is-dementia/types-of-dementia/frontotemporal-dementiaLinks to an external site.
Alzheimer’s Association. (2024). Stages of dementia. https://www.alz.org/alzheimers-dementia/stagesLinks to an external site.
McCance, K., & Huether, S. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier.
National Institute of Aging. (2023). Understanding different types of dementia. https://www.nia.nih.gov/health/alzheimers-and-dementia/understanding-different-types-dementiaLinks to an external site.
Sheppard, O., & Coleman, M. (2020). Alzheimer’s disease: Etiology, neuropathology and pathogenesis. Alzheimer’s Disease: Drug Discovery [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK566126Links to an external site.

Attached is the instructions and rubric. This assignement is for a discussion post that should be 1000 words or less, APA format that includes minimum two peer review references. Organize work with headings. The POI for this assignment is 
Does
utilizing the stepped-care model in children and adolescents with depression
decrease suicide attempts when compared to
those who use standard care.