Alzheimer’s Disease (AD), Is A Chronic Neurodegenerative Disorder That Starts Gradually And Increases Over Time (WHO) 2018.
Introduction
Alzheimer’s Disease (AD), Is A Chronic Neurodegenerative Disorder That Starts Gradually And Increases Over Time (World Health Organization 2018). The most common and early signs of Alzheimer’s illness are trouble in memorizing on recent occasions. As the disease increased, various other symptoms appear like changes in mood swings, confusion, the problem in language, loss of self-care management, behavioral issues, and loss of motivation (Burns., 2009).
If the person’s situation becomes severe, they take away from their family and society. Slowly, they lost body functions that may lead to death (Khyade., 2016). The progression rate of AD can vary; from various diagnoses, it is observed that the typical life expectancy is about 3-9 years. The major causes of Alzheimer’s disease are not fully understood. Approximately 70% of the disease risk is supposed to be a genetic disease. (Gauthier,2005).
Types of Alzheimer diseases
There are mainly three types of disease is present;
- Late-onset Alzheimer’s
- Early-onset Alzheimer’s
- Familial Alzheimer’s
Etiology
The neuropathological features of Alzheimer’s disease seem like senile plaques and neurofibrillary masses. The senile plaques appear first in the area of the brain that associate with cognition. After progression of disease, it spread to the other cortical regions of the brain. From the APP, amyloid p-peptide developed by two cleavage events; by the proteolytic activity of β-secretase development at one end of the Ap peptide and the γ-secretase develop on the other end.
Aβ appears toxic for the neuron directly or indirectly by the production of free radicals or by inflammation (Näslund.,2000). The second distinctive feature of Alzheimer’s disease is the amassing of the neurofibrillary tangles in the neurons.
Epidemiology
In epidemiological research, occurrence and prevalence are two main processes. In the United States, nearly 60% higher risk of Alzheimer’s disorder in the non-Hispanic white people. Hispanic people have a 30% lower risk as compared to non-Hispanic white people (Tejada-Vera., 2013).
Role of immune mechanism and inflammation in the Alzheimer Diseases
The role of the neuroinflammatory mechanisms in the development of Alzheimer disease explored by the Alzheimer Association Research in April 2015. The capability of innate immune cells mainly astrocytes and microglia mediate the neuroinflammation in Alzheimer diseases. In central nervous system illness and response to injury adaptive immune system play an important role. In Alzheimer diseases, communication among the PNS and CNS play an important role. Important challenges impeding the advancement of new therapeutic agents and strategies to overcome Alzheimer diseases.
Role of receptors in Alzheimer’s diseases
Through the N-methyl-d-aspartate receptor, excitatory glutamatergic neurotransmission is acute synaptic plasticity and survival of neurons. The excessive NMDAR activity causes excitotoxicity and endorses cell death, a fundamental potential mechanism of neurodegeneration followed in Alzheimer’s disease (AD)
Role of gut microbiota in Alzheimer disease
Several important processes are modulated by the gut microbiota comprising maturation of microglia and activation of neurogenesis, synaptic pruning, myelination and permeability of the blood-brain barrier. By metabolic, endocrine, neural, and immune pathways that are important for the maintenance of brain homeostasis. The microbiota-gut-brain axis connects the gut microbiota and the brain. Developing evidence shows that gut dysbiosis might exaggerate the Aβ accumulation and neuro-inflammation in the expansion of AD.
Gut dysbiosis
Gut dysbiosis decrease the beneficial substances,such as SCFAs and H2. They increase the permeability of the intestinal mucosal barrier and BBB. It stimulate the peripheral immune responses, and increasing the amount of peripheral and central oxidative stress. It observed that by increasing the amyloid plaque formation, insulin resistance, oxidative stress and neuro-inflammation gut dysbiosis contribute to the progression of AD pathology
Vascular dementia and Alzheimer disease
Vascular dementia commonly describes the problems like planning, reasoning, judgment, memory and various other processes that cause brain damage by decreased blood flow to the brain. Symptoms of vascular dementia are different according to the supply of blood to the various parts of the brain.
Diagnosis
The analysis of Alzheimer’s disease depends on the medical history of the patient. The history collected from the relatives and by the communication remarks.
Used Techniques
These advance medical imaging techniques are used for analysis of Alzheimer’s disease.
- Computed tomography
- Magnetic resonance imaging technique
- Single-photon emission computed tomography (SPECT)
These techniques help to predict the various stages of AD from mild to severe disease.
Prognosis
At an early stage, the diagnosis of Alzheimer’s syndrome is difficult. The symptoms of AD progress from mild cognitive problems to a severe mental disturbance that impossible to eliminate, in the late stage of AD. With Alzheimer’s disease, life expectancy reduced among people typically from 3-9 years (Zanetti.,2009). About less than3% of people live for beyond 14 years. This disease associated with compact existence and amplified cognitive damage, and a disturbance in the neurological examination. It observed that men have less survival prognosis in comparison to women(Mölsä.,1995).
Treatment
Current Alzheimer’s medicines help in the recovery of memory symptoms and other perceptive alterations. These drugs are used for the treatment of cognitive symptoms.
Cholinesterase inhibitors
- These drugs boost up the cell-to-cell message and reserve the chemical messenger.
- These drugs recover the neuropsychiatric symptoms, like depression and agitation.
Memantine (Namenda)
- The use of this drug helps to slow the progression of Alzheimer’s disease symptoms from mild to severe conditions. Sometimes this drug used in combination with other cholinesterase inhibitors.