p.p1 cognitive and basic neuronal functioning. This paper

p.p1 {margin: 0.0px 0.0px 0.0px 0.0px; font: 12.0px ‘Times New Roman’; color: #000000; -webkit-text-stroke: #000000}
span.s1 {font-kerning: none}
span.Apple-tab-span {white-space:pre}

The human brain is both intricate and delicate. Our minds are able to perform complex tasks while overseeing basic autonomic life-sustaining processes. Unfortunately, there are many diseases that affect both cognitive and basic neuronal functioning. This paper will discuss the effect of Alzheimer’s disease on cognitive functioning and memory, as well as promising current research on the disease. 
Alzheimers disease is the most common cause of dementia—the decline of cognitive and behavioral abilities to the extent that it interferes with normal functioning. The intensity of dementia varies from mild to severe—in which a person may be completely dependent on others for basic functions. The initial and primary markers of the disease are seen in abnormal beta amyloid plaques, neurofibrillary tangles and a reduction in neuronal connections. While the neurological symptoms and effects are known, scientists and clinicians are unsure of the causes of Alzheimer’s disease 
Memory decline is typically one of the first symptoms of cognitive decline in Alzheimer’s disease. The pathological neurofibrillary tangles that show up in brain images of patients with Alzheimer’s occur in the medial temporal lobe structures, such as the hippocampus. These tangles interfere with the neural networks crucial for optimal memory encoding, storage and recall. 
Our memories, specifically our autobiographical memory, allow us to be unique individuals, owning our personal experiences. Autobiographical memory consists of episodic memories—our specific recollections, and semantic knowledge—which is generally factually based  Alzheimer’s disease impairs autobiographical memory and is characterized by anterograde amnesia—the inability to create new memories, and retrograde amnesia—the inability to retrieve past memories. Unable to form new recollections, or remember old experiences, patients are at risk of losing their identity. In a study performed by Addis & Tippett in 2004, patients with Alzheimer’s were asked to answer questions about their sense of self. Results showed strong correlations between loss of autobiographical memory caused by Alzheimer’s and a lack of self identity. This can escalate to the point in which patients in the severe stage of the disease may be unable to recognize themselves in the mirror. 
Alzheimer’s disease impacts one’s executive functioning as well. Executive functions are higher-order control processes that regulate thought and behavior. This is controlled by the prefrontal cortex, and is what sets humans apart from other species. Results from multiple studies show that patients with Alzheimer’s have executive function deficits including planning, decision making, attention span, and organization. 
Alzheimer’s disease is a devastating illness, and, unfortunately, one that is still not fully understood. However, there have been great advances in the study of both the progression and treatment of the disease, and that has yielded promising results. As mentioned above, Alzheimer’s is marked by the accumulation of amyloid beta peptides (proteins) that form extracellular plaques in the neuronal tissue of patients. New therapeutic approaches are studying the possibilities of active and passive immunotherapy to treat and prevent further degeneration of nervous tissue by these plaques. 
The active immunotherapy focuses on attempting to program the patients’ own immune system to fight the plaque formation. This is done through introducing a fragmented version of the amyloid beta protein, which then spurs the immune system to create antibodies against it, much like a simple flu vaccination. Unfortunately, this active approach still poses a danger of adverse side effects to patients in the currently ongoing clinical trials, but shows potential as a possible prophylactic measure
The passive immunotherapy approach bypasses the danger of active immunotherapy and works against the amyloid beta proteins by introducing monoclonal antibodies, meaning antibodies cloned from a single parent cell.  Once they pass through the blood brain barrier, they work through three mechanisms. First, the antibodies aim to decrease the proteins’ ability to form toxic compounds. Second, the antibodies introduced signal the phagocytosis of the proteins, a process in which the proteins are engulfed by immune cells. Finally, the immune cells lyse, or burst, the proteins— destroying them both in structure and function (Barrera-Ocampo & Lopera, 2016).
Both the active and passive immunotherapies are currently the best approaches to preventing neurodegeneration and decline of cognitive abilities in patients with Alzheimer’s. However, more specific vaccines are needed with active immunotherapy to avoid harmful side effects to the patients. In regard to passive immunotherapy, more research is required regarding the efficiency of the antibodies to cross the blood brain barrier, as well as ensuring there is no harmful cross reactivity
A second exciting field of research revolves around the study of the acetylcholine neurotransmitter and the cholinergic system of the brain. Acetylcholine is a neurotransmitter used by all cholinergic neurons, and is crucial in both the central and peripheral nervous systems. The cholinergic system is involved in vital physiological mechanisms, including cognitive processes such as learning, memory, sleep, and sensory integration
Cholinergic transmission is an important factor of Alzheimer’s disease, and the pathophysiology of the disease leads to a major decline in memory and cognitive abilities. These cholinergic synapses are affected and damaged by the amyloid beta plaques that are present in patients with Alzheimer’s. Disrupting cholinergic information transmission to the cortex impairs the ability to make decisions and pay attention. Even more so, blockage of these cholinergic receptors impairs the encoding, storage and retrieval of information 
Regrettably, none of the drugs currently available to treat Alzheimer’s prevent the progression of the disease. New research focuses on the cholinergic system, to not only treat symptoms, but to treat the disease itself. These new therapeutic interventions include drugs such as memantine, which protects the cholinergic neurons. Donepezil, a drug used to inhibit the destruction of acetylcholine, is being studied and used to encourage cognitive and functional improvements. These are only a few of the many new drugs being tested with the aim to diminish amyloid beta production, salvage cholinergic neurons, as well as to avoid the loss of cortical and hippocampal neurons, all of which can prevent the progression of Alzheimer’s disease 
The suffering of patients, and loved ones of those with Alzheimer’s disease, is immense. The disease targets both the mind and body, stripping away the very things that make each one of us unique. The only consolation is found in the thousands of researchers working day and night to discover methods of prevention, management, and treatment of the disease. I am excited to see the future scientific advancements that will benefit patients, loved ones, and clinicians.