Introduction
Description of Alzheimer’s Disease
Dr. Alois Alzheimer originally used his patient Auguste D. to illustrate Alzheimer’s disease (AD) in 1906. The patient went through mental changes, memory loss, and a lack of trust. Dr. Alzheimer detected the shrinking in and around her brain’s nerve cells during the postmortem. Dr. Alzheimer also identified several unexpected side effects, such as difficulty speaking, unease, and disarray. First mentioned in medical writing in 1907, the disorder was named Alzheimer’s in 1910.
Individuals who occasionally forget where something is, struggle to remember names after meeting new people, cannot remember what someone did just a minute ago or have trouble organizing and sorting things. Such an individual needs a special dimension of concern in the second stage of Alzheimer’s due to the disease’s progression. One or more signs of the second stage include difficulty articulating thoughts and utilizing language. Other signs include being confused or acting strangely.
Research Topic and Aims
My topic is the early diagnosis and treatment of Alzheimer’s disease. This paper aims to cover the Early Identification of Patients in the Pre-Demented Stage of Alzheimer’s Disease and methods that can be used to detect it. Most often, dementia patients are also found to have Alzheimer’s disease (AD)(Luo et al., 2020).
The study, in this case, will help more seasoned adults to select their therapy and daily plans before the sickness worsens, thanks to new diagnostic techniques like MRI and PET scans. Thus, the patient can create living plans, such as choosing which home health agency or LTC office to work with in the future.
The effectiveness of several methods for spotting Alzheimer’s in its early stages is being investigated. This study aims to identify Alzheimer’s disease before dementia itself is determined and the methods that can be used to detect it. No therapies exist, but researchers are working to identify it earlier and slow its progression.
Research Design
The quasi-experimental design is used in this study’s experimental research design methodology. The study participants are not selected using randomization in this approach. Instead, inclusion is subject to a set of requirements. Researchers who employ quasi-experimental methods must make meticulously thorough, logical justifications for their decisions when excluding competing hypotheses from the possibility of explaining their findings of a causal relationship (Soria Lopez et al., 2019). Adding control or comparison groups, pretests, posttests, removing and reinstating treatments, replications, adding replications, reversing treatment, and case matching improve quasi-experimental designs.
Research Sample
This study has a single sample, which the researchers plan to split into two sections later. The task group for this French-based research project included researchers and clinicians from several clinics interested in memory problems (Scheltens et al., 2021). They developed a battery of neuropsychological tests to choose participants for this study.
The participants were picked on an outpatient basis from 14 different aging-related centers. Memory issues, a score of at least 24 on the MiniMental State Exam word recall, or equal to or less than 28 on the Isaac-set test, a score chosen by the clinicians on the PAQUID study, being at least 58 years old, speaking French, having completed four years of education, and having an informant or caregiver who could also help when necessary, with follow-up appointments for exams needed for the study were the inclusion criteria, according to the survey. Following the trial, the participants will receive follow-up care for three years.
Information on the 251 participants in this study was input using the ACCESS program. “SAS version 8.2 was used to conduct all statistical analyses. Means, standard deviation, and minimum and maximum values were reported in the descriptive statistics for each variable. Furthermore, evaluated were the associations between each neuropsychological score and sex, age, and educational level.
Research Purpose and Ethics
The purpose of the study over three years was to see whether these neurological tests offered early information that could be applied to diagnose patients more broadly. Each participant provided their informed consent at the start of the study for both the initial testing and the post-study follow-up.
Other ethical guidelines used were obtaining institutional approval, having reviewers, reporting study findings, and publishing research findings. By doing this, it is ensured that impartial parties evaluate the data per the set standards. The same battery of tests is administered to monitor disease progression at every six-month checkup (Pais et al., 2020). There is no need to lie during the testing phase because no medicines are administered. This research aims to determine how and how early a diagnosis can be established.
Neuroimaging
Brain imaging tools non-sly explain the neuropathological mind progressions in vivo constitutional and working information. Constitutional imaging uses both CT and MRI to adequately depict the architecture and morphology of the brain. Structural brain imaging results establish a connection between neurodegeneration and the various aspects of AD (Jiang et al., 2019). Functional imaging is therefore used to study how the brain controls things like blood flow, chemical properties, and body metabolism. The most effective imaging technologies, such as fMRI or PET imaging using the tracers F-fluorodeoxyglucose (FGD-PET) and C-Pittsburgh Compound-B (Pib-PET), are used primarily to find new AD biomarkers.
Imaging Using Magnetic Resonance (MRI)
Blood flow patterns and metabolic rate are two key indicators of brain function; magnetic fields are used to align and calculate the reverberation frequencies that evaluate the blood flow rate. Compared to MCI patients, AD patients have less neuronal activity in the orbitofrontal gyrus and the medial prefrontal cortex (Guzman-Martinez et al., 2021). The broad default-mode network in the human body or autogenic ideas in humans are caused by these two areas. A progressive decline in brain activity in AD patients mirrors the weakening of the default-mode network caused by the illness condition.
Using structural MRI (sMRI), early AD weakening can be distinguished from typical aging weakening. AD degeneration begins and spreads to the temporal neocortex in the medial temporal lobe, hippocampus, amygdala, and entorhinal cortex. Degeneration was found in AD patients at a rate of about 3 to 5% per year, which is relatively low compared to 15 to 25% per year in moderately afflicted patients, suggesting that degeneration occurs before diagnosis (Grossberg et al., 2019).
Cognitive function declines as a direct result of brain degeneration, suggesting that volume markers may be employed to track disease progression. Interestingly, the MRI distinguishes between AD and healthy patients with a reasonable degree of precision. With MRI, it is simple to detect deterioration in the medial temporal lobe’s constituent parts, including the hippocampus, in preclinical episodes of AD.
The MRI also shows how the infection progressed from cognitive normalcy to moderate cognitive impairment (MCI) and then to Alzheimer’s disease (AD (Khan et al., 2020)). With research showing a 10-15% decline in MCI from the level of healthy people, the shrinkage of the hippocampus is associated with the onset of the disease. With mild dementia in AD, the reduction values are 15–30%, but for moderately or severely affected individuals, the reduction values are 15–40%.
Research shows that the sMRI can predict the translation to AD with an accuracy of about 80%. Including joint biomarkers allows for the most significant transition prediction from MCI to AD. Furthermore, the common biomarkers effectively predicted the conversion by combining complicated measurements of diffusion computations with grey matter volume and a complex calculation of CSF proteins (tau/Ab42 ratio), allowing them to assess 91% of amnestic MCI victims precisely.
The best biomarker for the AD structure for brain imaging, particularly in the early diagnosis of the condition, has been determined to be hippocampal volumetry. The measurement software appears sufficiently available, making it the ideal machine for MCI patients to employ in their risk reduction efforts and for AD sufferers seeking treatment in the early stages of illness development (Malaiya et al., 2022). Hippocampal volume remains a key systemic metric for assessing the disease’s progression in AD, although machines are now preferred for research rather than clinical screening.
Tomography Using Positron Emission
PET imaging uses cellular metabolism to map brain activity. Covalent bonds are created between radioactive tracers and molecules like glucose, which the body ingests and degrades. Due to the collisions between positrons and electrons, the emitted tracers encourage the release of gamma rays. Computer-generated images in two- or three-dimensional hues are generated to trace AD variations based on the magnitude of the visible gamma rays that follow (Ismail et al., 2020). Patients are given radioactive amalgam in modest doses before scanning; this amalgam contains isotopes that release positrons. The resulting collision between the positrons and the electrons produces gamma rays, which the PET records as “coincidence events.”
Using the radiotracer amyloid-beta, PET imaging is crucial for identifying both Ab plaque deposition and neurodegeneration (PiB). Since amyloid lesions can develop in both dementia structures, PiB-PET has lower specificity but still accurately detects, analyzes, and forecasts the health status of AD patients (Clay et al., 2020). Compared to the FDGPET, the approach of amyloid imaging has fewer longitudinal investigations, making it essential. To diagnose AD patients, the radiotracer 2-(18F) Fluoro-2-deoxy-D-glucose (FDG) can be used to measure the amount of glucose used in the brain.
The FDG-PET has a great sensitivity to early pathological symptoms. The metabolic deficits documented by the technology are also present in other forms of dementia. Therefore, its specificity is limited. Furthermore, [11C]PiB and [18F] florbetapir disclose the brain regions and separate the amyloid-containing areas from the surrounding tissue, precisely like the PET imaging that reliably conducts the AD diagnosis (Tertullian, 2022). A pattern is revealed in the brain regions (Frontal et al.) of AD patients with increasing [11C]PiB. This demonstrates the established relationship between imaging evaluation and the immunohistochemistry test, validating the use of amyloid imaging in clinical research.
Identifying amyloidosis in NCI geriatric people and MCI patients allowed for predicting the transition to AD and enhanced understanding of the clinical course. For instance, the [11C]PiB scan indicates the conversion to AD from MCI, with 55% of [11C] PiB-positive victims of MCI converting to AD in 2 years compared to 10% of [11C]PiB-negative patients. In a year of observation, the translation rate from MCI to AD increased due to the high retention rate in [11C]PiB. Even though there is a known correlation between the brain amyloid and CSF-Ab in AD patients, measurements show that different self-autonomous processes that arise at different disease levels are partially visible.
Conclusion
A lot of research has been done on Alzheimer’s. There is no one method to attempt to understand this enormous disease and its various issues. Psychologists and researchers frequently share their findings and build on the work of others. Every day, new medical treatments are being evaluated. “Using MRIs, researchers are looking for vascular anomalies in the brain that could be signs of Alzheimer’s disease. The benzodiazepine medication lorazepam may be used to detect Alzheimer’s disease in its early stages. Neuroimaging could help determine whether these individuals are at increased risk for brain amyloid.
Recent empirical evidence suggests that people with Alzheimer’s disease have changed levels of the amyloid blood biomarker. A high levels of IL-10 and IL-12/23p40, as well as other biomarkers like Eotaxin-3 and Leptin. That implies that researchers may be able to identify the preclinical stage of Alzheimer’s disease using a blood-based panel employing cumulative data from highlighted biomarkers to enable preventive medication before irreversible neurodegeneration begins.
The preclinical diagnosis of AD symptoms is aided by the development of new technology and platforms that can detect a high density of various types and levels of biomarkers in the bloodstream. To identify the source and treatment of an illness that is both socially and economically expensive, researchers are making good progress.
In support of the rationale, Romans 5:12–15 explains that because we all sin in front of God, sin entered the world through one man and brought death to all of us. We all lost our perfection and were doomed to death due to Adam’s sin. Sin-related sickness prevents the brain and body from regenerating as God intended when he made the first man.
Neuroscience is a gift from God, who gave men all the wisdom they possess. God’s plan for us is to be rescued by grace today, and because of the death of his son on the cross, we are all qualified to spend eternity with him. Our messiah wants to use human intelligence to foster creation rather than destruction; because of this, neurophysiology and neuropsychology align with God’s will.
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