Reconsidering Alzheimer’s Pathology and Hippocampal Neurogenesis.

Genes manipulate the function of every cell in our bodies, including basic characteristics and potential disease development. The genes that determine potential disease development can make someone more prone to developing Alzheimer’s. The gene that is associated with AD is called apolipoprotein E, also referred to as APOE; there are three different types of APOE, but only one has been shown to increases the risk of AD, it is referred to as APOE e4. We each inherit an APOE form our mother and fathers, having even one APOE e4 gene increases the risk of developing AD. If a patient has two APOE e4 genes, the risk is even greater.

Presenilin Mediated Disruption of Intracellular Calcium Homeostasis in the Pathogenesis of Familial Alzheimer’s Disease. Introduction Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive cognitive decline resulting in memory and language deficits, personality changes, and gradual loss of independence. AD is the most common form of age related dementia, effecting over 5.2 million Americans age 65 years and older[1, 2]. Most cases of AD are idiopathic in nature, however a rare variant, Familial Alzheimer’s Disease (FAD), is related to autosomal dominant mutations in one of three genes: amyloid precursor protein (APP), Presenilin-1 (PS1) or Presenilin-2 (PS2). Representing less than 5% of all AD, FAD is characterized by an early age of onset (<65), and accelerated progression.

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Patients with type A, the infantile form have 0.7% of the normal sphingomyelinase activity with median values in the range of 0-1% , while in patients with adult onset neuronopathic or non-neuronopathic disease the activity range is 0-19% of the normal, with median values in several tissues from 2-8% . This enzyme defect explains the massive deposition of sphingomyelin in tiss... ... middle of paper ... ...sh Medical Journal: 295(6610):1375-1376. 4. Levade, Salvayre, Maret and Blazy. Endogenous and Exogenous Sources of Sphingomyelinin Pick’s Disease A & B.

The neuropathologic examination of the brains with visual impairment in the Hof et al. (1997) study revealed cortical atrophy dominating on the posterior parietal cortex and occipital lobe(Hof et al.). A study by Beta-amyloid is considered an important factor in AD and was shown to be the major cause in senile plaques. Acetylcholine A number of neurotransmitters and neuromodulators, including acetylcholine (ACh), somatostatin and glutamate have been found to be deficient in Alzheimer's disease (AD).