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Transcript of Alzheimer's disease
Neurofibrillary tangles - twisted fragments of protein within nerve cells that clog up the cell
Neuritic plaques - abnormal clusters of dead and dying nerve cells, other brain cells, and protein
Senile plaques - areas where products of dying nerve cells have accumulated around protein
When neurons are destroyed, there is a decrease in the chemicals that help nerve cells send messages to one another - neurotransmitters.
Areas of the brain that normally work together become disconnected.
Changes? What changes:
especially severe in the hippocampus cortex shrivels up damages: thinking, planning, remembering ventricles grow larger Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells. beta-amyloid proteins - chemically sticky - "clog" the plagues Tau hyperphosphorylation Vascular hypothesis Critically
Hypoperfusion genetics, oxidative stress, dysfunctional calcium homeostasis, hormonal, inflammatory-immunologic, and cell cycle dysregulation Neurotransmitter Dysfunction hypothesis Neurotransmitters involved Treatment of Alzheimer's No specific treatment, but slowing the rate of disease progress Medication Other techniques and social support Donepezil (Aricept)
Galantamine (Razadyne, former Reminyl)
Other medications Acetylcholinesterase inhibitor
Increase the levels of Acetylcholine
Block ion channels (memantine)
BUT!!! Severe side-effects
Stimulate brain activity (board games, crosswords)
Stimulate social interaction (friends, communication with other people) Stimulate creativeness (drawing, painting, playing musical instruments) Social support for patients and for people that surround them is ESSENTIAL!!! References Used Alzheimer's Association National, (2011). Stages of Alzheimer's. Retrieved February 27, 2011, from http://www.alz.org/alzheimers_disease_stages_of_alzheimers.asp
Hardy, J., & Selkoe, D. J. (2002). The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics. Science, 297(5580), 353. Retrieved from EBSCOhost.
Mohandas, E. E., Rajmohan, V. V., & Raghunath, B. B. (2009). Neurobiology of Alzheimer's disease. Indian Journal of Psychiatry, 51(1), 55-61. Retrieved from EBSCOhost.
National Center of Biotechnology Information US, (2010). Alzheimer’s Disease Senile dementia. Alzheimer’s type. Retrieved February 27, 2011 from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001767
Neurology and Psychiatry: Alzheimer's Disease and Other Dementias. (2003). Current Medical Literature: Health Care of Older People, 16(2), 40. Retrieved from EBSCOhost.
most damaging - groups (block sygnaling in the synapsis) activate immune cells = trigger inflammation in healthy brains - tau protein forms nice parralel tracks in Alz brain - forms twisted tangles tracks disintegrate, can't stay straight, block nutrient supply to neural cells * by Olya Bartiuc, Alla Khoruzha, Aleksejus Petrila
Thanks. Questions? Acetylcholine Norepinephrine Dopamine Glutamate (NMDA receptors) Others (neuropeptides, estrogen)