Mini-Mental State Assessment ( Kirbas Et Al )

The occipital lobe is in a posterior position and the function of the occipital lobe is vision including perception and colour and movement (Stannard Gromisch, 2012). Atrophy is described as a process of tissue wastage or cell death (Lippincott Williams & Wilkins, 2006). According to (Jones & Gaillard, 2005-2013) the pathology of PCA includes Neuritic plagues and neurofibrillary tangles which are found in the parieto-occipital and temporo-occipital areas, as well as occasionally in the primary visual cortex. It is thought that PCA is a version of AD, with very little difference in the pathology. “Neuritic plagues or senile plagues are extracellular and composed of a central core of beta-amyloid peptides aggregated together with fibrils of beta-amyloid, dystrophic neurites, reactive astrocytes, phagocytic cells, and other proteins and protein fragments derived from degenerating cells or liberated from neurons” (Weerakkody & Gaillard, 2005-2013).

When testing for Alzheimer’s, a patient must show a decline in at least two of these categories, which is significant enough to interfere with regular function. Alzheimer’s specialists have been working on new ways to diagnose the disease as early as possible. Specialists have discovered that they can measure the amount of beta-amyloid in the cerebrospinal fluid (Chertkow, etc. all, 2013). These “sticky” beta-amyloid plaques that build up in the brain have been proven to affect memory. It is now known that the buildup of these plaques can cause nerve cell damage (Nierenberg,

As the population keeps aging, Alzheimer 's Disease (AD) is becoming a more significant public health issue. The prevalence of AD is expected to reach 34 million worldwide by 2025 (Mount 2006) and with the aging demographic, early diagnosis and treatment of AD is gaining importance. Cognitive decline and altered brain function related to AD has been shown to be present years before the clinical onset of the disorder through functional brain imaging techniques (Prvulovic 2011). Emphasis has been on detection of AD in its preclinical stages to provide early interventions for the patients. Since Fuld et al.(1990) 's study suggesting that the examination of cognitive functioning in non demented older adults is predictive of prospective dementia, countless studies have attempted to devise reliable methods of detecting cognitive changes and risk factors in preclinical populations.

structures. These then cause the neuronal cell death and loss of synaptic function that occurs in AD (Laferla).

Many physiologic changes contribute to AD. Currently, theories related to the changes that cause AD include the following: “Degeneration of the cholinergic neuron and deficiency in acetylcholine, neuritic plaques that form mainly outside the

The evidence of neurofibrillary tangles is important to diagnosis. Inside the neurons, there will be abnormal clumps of tau protein. Tau protein normally attaches to microtubules of the neuron and acts as its stabilizer. Abnormal chemical changes cause Tau proteins to detach from the microtubules and stick to other tau proteins, forming threads, which clump together—tangles. Tangles may block the synaptic signaling between the neurons. Neurons will eventually begin to die and as this spreads, regions begin to shrink. The final stage will have widespread damage and significant shrinkage. Scientists are looking for specific types of cell death, which are found in normal aging, but greater in AD and the location matters. The brain will also show signs of inflammation in response to cellular injury (22, 23).

FINDING GENES Causes of AD include extracellular neuritic plaque and intracellular neurofibrillary tangles. The plaque has amyloid-[beta] peptides (Tanzi, 2001). A protein called tau makes tangles

The brains of AD patients display characteristic 'plaques' and 'neurofibrillary tangles', the proliferation and abnormal formation of these abnormal proteins is the basis of the processes which cause AD.  Apolipoproteins enhance the breakdown of beta amyloid in the brain.   APOE4 which was mentioned earlier as the main risk factor, is a variant of these proteins which is less effective at breaking down beta amyloid than the others in it's class.  This explains why individuals with one or two alleles for APOE4 have a notable build up of beta amyloid surrounding the neurons of the brain.  A substance called amyloid precursor protein (APP) is found penetrating the cell membranes of properly functioning neurons, which helps neurons grow, function, and repair damage that occurs.  Through interaction with an unknown enzyme, APP is broken down into shorter segments which form 'fibrils' of beta amyloid which clump together outside of the neurons and eventually progress to form the 'plaques' of AD. Excess beta amyloid is believed to alter the calcium homeostasis of neurons which is believed to induce increased apoptosis of neurons, leading to an overall loss of neurons over time.  Beta amyloid is also found to build up in, an inhibit proper function of the neuronal mitochondria, interfering with normal glucose metabolism which leads to neuron death and loss of brain volume (this is why brain imaging of these patients shows decreased glucose metabolism).  The beta amyloid is predominately thought of as an extracellular

An estimated 24 million people worldwide have dementia, the majority of whom are thought to have Alzheimer's disease. Thus, Alzheimer's disease represents a most important public health apprehension and has been recognized as a research priority. It begins with memory loss of trouble with language skills and increase into irritability and angry outbursts. Because of its degenerative nature the disease leads to full blown dementia and loss of even basic motor skills as the patient drifts further and further away from their more natural and normal selves. Recent developments in neuroimaging techniques provide great potentials for effective diagnosis of Alzheimer ’s disease (AD), the most common form of dementia. Previous studies have shown that

In medicine, an early diagnosis can mean the difference between life and death. With today’s advancements in technology, early diagnosis is becoming a real possibility for many diseases, including Alzheimer’s disease. Worldwide it is estimated that 24 million people have dementia, the majority of these people are thought to have Alzheimer’s disease. (Mayo Clinic, 2014) According to Alzheimer’s Foundation of America (AFA) (2015) Alzheimer’s disease is among the top ten leading causes of death in the United States. Affecting 5.1 million Americans. Alzheimer’s disease is not a normal part of aging, but the risk of developing this disease increases with age. One of the best tools for diagnosing Alzheimer’s is magnetic resonance imaging

The neuropathological hallmarks of AD are the presence of plaques and neurofibrillary tangles. (18 -20)

(Seyedabadi, 2014 as cited by Boulougouris & Tsaltas, 2008; Kiser et al., 2012; Meltzer et al., 2012). The cause of AD can be associated with many mutations; one specific mutation is in the amyloid precursor protein (APP). The amyloid protein in normal functioning is 40 amino acids long. In AD, this amino chain is 42 amino acids long and cut in the wrong places. Some serotonin modulators are associated with this change in the expression of APP (Seyedabadi, 2014 as cited by Payton et al., 2003; Postina, 2012).

Prior to advances in imaging, the primary means of diagnosing AD is from the patient history and cognitive impairment testing (Long, Chen, Jiang, & Zhang, 2017). Interviews with the family members and caregivers are part of the assessment (Long et al., 2017). The diagnosis based on neuropsychological scale is subjective and less repeatable and a rich clinical experience of physicians is required (Long et al., 2017). The presence of neurofibrillary tangle, plaque buildup and tissue loss in the brain parenchyma indicates the progressive degenerative nature of AD (Long et al., 2017). Early detection of the disease is crucial in the patient management (Long et al., 2017). Short-term memory loss and paranoia are the earliest symptoms

A standout amongst the most energizing methodologies of treatment is utilizing β-amyloid antibodies to assault the malady. Discovering approaches to let down levels of β-amyloid is a key step towards the curing AD, and hereditary qualities assumes a significant part in this procedure. A change in the quality Apoe that advances the arrangement the β-amyloid into neuritic plaques is the initially ensnared in the hereditary qualities of the illness. Understanding the first occasion that happens, and what happens to a well-working cell to prompt the onset of the sickness is essential (The Alzheimer's Project, 2009). The larger part of individuals diagnosed with AD have the late-onset variations. Then again, concentrating on the early-onset cases has been the best hotspot for exploration in discovering a cure for the

Our understanding of the molecular underpinnings of why AD is a memory disorder has increased significantly during the past 15 years. For decades, it was thought that neuritic or senile plaques,