Hippocampal Atrophy Experiment

When substances like Acetylcholine (Ach) and norepinephrine which are small- molecular neurotransmitters are released into the body they bind to receptors on tissue or neurons through our ANS and PNS system. Ach is released by many PNS neurons and some CNS neurons. In the PNS Ach is an excitatory neurotransmitter at some synapses, such as the neuromuscular junction where it binds to ionotropic receptors which open cation channels. Ach can also be an inhibitory neurotransmitter at other synapses, where it binds to metabotropic receptors while opening potassium channels. The enzyme acetylcholinesterase (AchE) inactivates Ach by splitting into acetate and choline fragments. Norepinephrine (NE) is a biogenic amine; most biogenic amines may cause

and Mattson, 2011), and impairments of axonal transport and mitochondrial functions (Decker et al., 2010; Querfurth and LaFerla, 2010; Sheng and Cai, 2012). In addition, several lines of evidence suggest that Aβ regulates neuronal and synaptic activities and that its accumulation in the brain causes aberrant network activity and synaptic depression (Palop and Mucke, 2010). Impairments of inhibitory interneurons and aberrant stimulation of glutamate receptors result in excitotoxicity, and play important upstream roles in this pathogenic cascade. These impairments also lead to a positive feedback loop, where aberrant neuronal activity augments Aβ production, which in turn leads to further neuronal damage (Palop and Mucke, 2010; Bero et al., 2011; Verret et al.,

A plausible explanation for the thinning of the RNFL in AD is death of retinal ganglion cell axons, and retrograde degeneration due to further loss of cortical neurons. The damage to these cells could be caused by the neurotoxicity of the Aβ aggregates formed during AD. Scientific findings have shown that AD affects the eye, and more specifically produces

Black has stated that genetic causes often involve the mutation of multiple genes and have identified at least five chromosomes: 1, 12, 14, 19, and 21 (Black, 2009, p. 1894). Four genetic loci have also been identified as contributing to AD, including the amyloid precursor gene, the presenilin 1 gene, the presenilin 2 gene, and the apolipoprotein E gene on chromosome 19. Though there is not enough conclusive research to directly link AD to environmental factors (such as toxins or head trauma) or personal health (diabetes, vascular disease, heart and stroke), these issues are known to contribute to the destruction of brain cells. Understanding the etiology of brain cell loss is relevant to understanding how to effectively prevent the loss of function in the brain. For example, preventing the formation of chemicals called free radicals with antioxidants can indirectly prevent AD. Other causes of brain cell loss include a neurotransmitter called glutamate and an accumulation of beta amyloid proteins. Therefore, although the cause of AD has been unidentifiable, many contributing factors have been observed.

Paranoid Schizophrenia can come on quick suddenly and disrupt a person’s normal daily functions. People suffering from paranoid schizophrenia prominently experience delusions and hallucinations. Some individuals can be predisposed to schizophrenia due to cortical atrophy hypothesis or the dopamine hypothesis. Cortical atrophy hypothesis believes that the patient’s brain size can cause schizophrenia, while the dopamine hypothesis argues that levels of dopamine in the brain are directly related to the onset of schizophrenia.

Amyloid beta is also associated with reduced levels of the neurotransmitter protein acetylcholine. An acetylcholine receptor is an integral membrane protein that forms part of essential processes like memory and learning, which are progressively destroyed in patients with Alzheimer's disease (Qué es la enfermedad de Alzheimer?, n.d., para. 6).

In addition, decreased cerebral blood flow, environmental toxins and a decrease in acetylcholine have all been labeled potential culprits. Various theories for the cause of Alzheimer’s have been put forth but as yet none have been shown true.

As the progressive disease take over the body, the ability to function, understand, and comprehend becomes an issue. On a neurological level, the disease affects the brain causing senile plaques and neurofibrillary tangles to build and connect between the cells. The plaques contain proteins that are called beta-amyloid that clump together between the nerve cells. On the other hand, tangles are twisted strands that keep

Earlier research was done on the inhibition of amyloid β, but a relatively new approach is to find inhibitors for acetlycholinesterases enzyme (AChE). The action of AChE results in the blockage of transmission of acetylcholine (ACh), hence hyperphosphorylating the tau protein which affects the breakage of amyloid precursor protein(APP), which firther results in the increase in amyloid β. The binding of AChE causes decrease in the binding of ACh to muscarinic recptor and nicotinic receptors (Francis, Palmer, Snape et al., 1998). A recent study has shown that ACh does not only have cognitive functions, it regulates the

The epsilon4 allele of apolipoprotein E4 (ApoE4) which is located in chromosome 19 is linked to the onset and progression of AD. The synaptic loss is due to a loss of cholinergic neurones which transmits nerve signals in the brain which are known to be linked to memory formation (figure 2). Amyloid plaques cause this loss.

- A chemical called acetylcholine is diminishing in the brains of people with Alzheimer’s disease. It’s one of the many chemicals that nerve cells use to communicate and is a neurotransmitter that plays a critical role in memory and learning

Alzheimer’s disease is a neurodegenerative disorder, it affects two pathological hallmarks: amyloid plaques and neurofibrillary tangles. “Amyloid plaques are caused when protein pieces called beta amyloid stick together, they eventually build up between the nerve cells into plaques.” (Ballard, 2011) Amyloid plaques trigger neurological dysfunction and eventually brain death. Compared to a healthy brain the amyloid is broken down and disposed, however in AD they collect and form hard plaques. “Once brain death happens there is no way for the brain to communicate, or restore memory” (Brightfocus.org, 2014). Neurofibrillary tangles are fibers found in the brain cells, and they have a primary protein called ‘tau’ which aids in the structure called microtubule. “Microtubules help move nutrients and other factors from one cell to another with Alzheimer’ the ‘tau’ protein is abnormal and the microtubule structure collapses.” (Ballard, 2014 & Brightfocus.org, 2014) Even though we often see the effects of AD on the outside; it is a neurodegenerative disease effecting the amyloid plaques and

The areas of the brain that are opulent in cholinergic neurons are vital areas for memory and learning (Hippocampus), attention and motivation (anterior cingulate), and the control of behaviours (hypothalamus). Most drugs that are used to treat AD are cholinesterase inhibitors. Cholinesterase inhibitors act by inhibiting the job of cholinesterase, they also work as an enzyme thus metabolising acetylcholine in the synaptic cleft, leading to more activity in the cholinergic synapses. Therefore the justification of using of these types of drugs is to decrease the shortage of cholinergic in synaptic diffusion thus restoring cholinergic operations or at the very least slow down the deterioration, (Parrott A, Morinan, A, Moss, M, Scholey, A. Wiley 2004).

Alzheimer's disease is a chronic, neurodegenerative disorder that attacks the brain’s neurons, resulting in loss in memory, destruction of thinking and verbal skills, and changes in behavior (Kerr & Small, 2005). It is known as the most common factor of promoting dementia after the age of 65. Besides, the estimation of dementia sufferers is 24 million people in the beginning of 21st century, and it is assumed that the figure may rise threefold by 2040 (Kawas, 2003; “The three stages of Alzheimer's disease”, 2011). This essay will discuss biological features of Alzheimer's disease in neurological, cortical and physiological perspectives. It will then evaluate how the progressive damage that may lead to cognitive impairment. Finally, some

For example imbalances in acetylcholine can cause the development of myasthenia gravis, a disorder that causes weakness in muscles and fatigue (“Acetylcholine”). Another example is the fact that an imbalance of acetylcholine and dopamine, can cause Parkinson's disease. Acetylcholine works with dopamine — neurotransmitter linked with mood and the sensation of pleasure — to smooth out movements so when there is an imbalance it causes shaky movements, which is a key trait of Parkinson's disease (“Acetylcholine”). Even damage to the certain parts of the brain that produces acetylcholine, such as the cholinergic portion of the brain, is linked to cause the development of Alzheimer's disease; the varied levels of acetylcholine is common in Alzheimer's patients. The lack of acetylcholine, specifically in the hippocampus can cause dementia; although, an abundant amount of acetylcholine can cause depression