Neurons with amyloid plaques.
 

Alzheimer’s Disease: a brain disorder that usually starts in late middle age or old age and gets worse over time. Symptoms include loss of memory, confusion, difficulty thinking, and changes in language, behavior, and personality. (NCI3) A “degenerative” disease whose fundamental cause is dying and damaged cells. (Ratey, 49) First appears as progressive "memory" loss and later develops into generalized dementia. (Kolb, 170) "Beta-amyloid plaques" and "tangles" of proteins inside neurons are characteristic features of brain tissue in patients with Alzheimer’s. (Fields,  311)

Relentlessly robs its suffers of their memories and "personality." 4.5 million Americans have this “neurodegenerative” disorder. Found in nearly half of those older than 85. Preventing Alzheimer’s at an early stage may be the only hope for those at risk. Marijuana may stall the disease. (SAM April/May 2007, 14) Alzheimer's One study showed that our chances for developing Alzheimer’s drops 17% for every year of education we have beyond high school. (Ratey, 231) Some of the most disturbing changes caused by Alzheimer’s disease occur when blood flow, activity, and neuronal connections in the “association cortex” are compromised. (Bainbridge, 264) In the early stages of Alzheimer’s, the symptoms of memory impairment are often mild, such as forgetting the names of familiar people, forgetting the location of familiar places, or forgetting to do things. As the disease progresses, memory loss and confusion become more pervasive. The person becomes unable to remember what month it is or the names of family members. Frustrated and disoriented by the inability to retrieve even simple information, the person can become agitated and moody. In the last stage, brain damage is widespread. The person no longer recognizes loved ones and is unable to communicate in any meaningful way. (Hockenbury, 252) Most cases of early-onset Alzheimer’s disease are caused by gene mutations that can be passed from parent to child. Researchers have found that this form of the disorder can result from mutations in one of three genes: ‘APP,’  ‘PSEN1,’ or ‘PSEN2.’ When any of these genes is altered, large amounts of a toxic protein fragment called ‘amyloid beta peptide’ are produced in the brain. This peptide can build up in the brain to form clumps (of) amyloid plaques. A buildup of toxic amyloid beta peptide and amyloid plaques may lead to the death of nerve cells and the progressive signs and symptoms of this disorder. (GHR)


Beta-Amyloid Plaques: dense deposits of protein and other cell materials outside and around neurons. Found in abundance in Alzheimer’s patients. (Hockenbury, 252) Clumps of the abnormal proteins. Build up in certain organs. This reduces their ability to work correctly. (PubMedHealth2) A … form of ‘amyloid beta-peptides’ is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with “Down syndrome.” The peptide is found predominantly in the "nervous system," but there have been reports of its presence in non-neural tissue. (MeSH) Alzheimer’s signature beta-amyloid crystals and micro-fibrillary tangles, that are killing off brain cells, are easily revealed in brain images in about half of normal 70-year olds. Yet, by their 70th birthdays, only 7% of people have received a formal Alzheimer’s or related “senile dementia” diagnosis. Sadly, the pathological seeds of greater troubles have already been planted in the majority of their 70-year old brains. (Merzenich, 5)

Neurofibrillary Tangles: twisted fibers that build up inside the neuron. Found to a great extent in Alzheimer’s patients. (Hockenbury, 252) A “pathological” accumulation of paired (protein fibers) composed of abnormally-formed ‘tau protein’ that is found chiefly in the “cytoplasm” of nerve cells of the brain and especially the “cerebral cortex” and “hippocampus.” Occur typically in Alzheimer's disease. (GHR) Abnormal structures located in various parts of the brain and composed of dense arrays of paired “neurofilaments” and “microtubules.” As one of the hallmarks of Alzheimer’s disease, the neurofibrillary tangles eventually occupy the whole of the cytoplasm in certain classes of cell in the cerebral cortex, hippocampus, “brain stem,” and “diencephalon.” The number of these tangles correlates with the degree of “dementia” during life. Some studies suggest that tangle “antigens” leak into the “circulation” both in the course of normal aging and in cases of Alzheimer’s disease. (MeSH)