Human Aging, Position Paper
Longevity of adults has changed little
Senior runners postponed disability 8.7 years
Estrogen with progesterone lengthens women lives
Testosterone and vascular functions in aging
estrogen and longevity
Free radicals part of aging process
FAD AGING CURES EXPOSED, by leading scientists
genes that slow aging
Genes and aging
Insulin's effect upon the SKN-1 gene and aging
Telemores, sexual size dimorphism and gender gap in life expectancy
SKIN AGING: causes & treatments
Carbohydrates and aging and age related diseases
Arthritis reduced with vigorous physical activity
Why Women Live Longer than Men

Genetic diseases which strike those past the age of reproduction and net positive contribution to society are not removed from the gene pool through natural selection.  Alzheimer is the principle one.


Since pasting this article of become very aware of the role of glycation (sugar molecule attaching randomly to amino acids and thereby compromising the functions of the protein) and in particular that of fructose is 7.5 times more reactive than glucose.  The evidence strongly supports the role of our excessive consumption of sugar, made worse by our high carb diet as responsible for the 10 fold rise in the rate of Alzheimer’s disease.  This diet overwhelms our biological system to repair the damage by glycation.    



Alzheimer’s & Vascular Dementia

Sources Merck Manual Eighteenth Ed, 2006; Wikipedia.org, Conn’s Current Therapeutics, 2002

Alzheimer’s disease (AD) is the 7th leading cause of death; 65,829 listed in 2004, and accounts for at least 50% of the progressive dementia. The next most common is vascular dementia, followed by Lewy body disease, and alcohol-related dementia.  It is the 3rd most costly disease. .  Sudden onset is not consistent with AD. Focal neurological findings {local damage}, seizures, periods of steady improvement, wide swings in abilities, and gait disturbance are features that are rare early in the course of the disease.  AD is twice as common in women as men (partly because they live longer), 30% above the age of 85; 45% by the age of 95.  AD is confirmed by autopsy in about 85% of those diagnosed with Alzheimer’s.  Every 5-years after the age of 65, the probability of being diagnosed with the disease doubles.  5-15%of AD is familial (5% for early onset with mutation of 3 different genes being involved).  At least 5 chromosomes influence outcome: 1, 12, 14, 91, & 21.  The risk of AD is substantially increased in those who have two E4 alleles, and decreased in those with the E2 allele, which codes for the apolipoprotein (apo) apo E.  .  30% of the U.S. population has one copy, and 11% two copies.  By the age of 70 those with two E4 (E4/4) alleles, 50% will have AD; while 28% of those with E3/4, and 6% of those with E2/4.  Some with apoE4 live into their ninth decade with no signs of dementia.  Apo E influences β amyloid deposition, cytoskeletal integrity, and efficiency of neuronal repair.  However, the Apo allele accounts for only about 30-50% of the genetic picture. 80% of cases involve known genetic risk factors.  Over 400 genes have been tested for association with late-onset sporadic AD.  Nearly 200 different mutations in the presenilin-1 or presenilin-2 genes have been documented in over 500 families. Mutations of presenilin 1 (PS1) lead to the most aggressive form of familial AD.  Over 20 different mutations in the amyloid precursor protein (APP) gene on chromosome 21 can also cause early onset of the disesase.  The pensenilins have been identified as essential compoents of the protelotic processing machinery that produces beta amyloid peptides through cleavage of APP.  Most mutations in the APP and presenilin genes increase the production of a small protein (peptide) Abeta42, the main component of senile plaques in the brins of AD patients.  The disease results from a protein misfolding of β amyloid or tau proteins.  β amyloid (βA) is thought to be involved in neuronal development.  The failure of βA to be remove results in dense diffused plaques and sometime also in the walls of small blood vessels (amyloid angiopathy).  The tau protein is involved in a different pathology.  They normally act to stabilize microtublules in the cell cytoskeleton. 


Life expectancy of patients diagnosed with AD is 7-10 years, with extreme survival of up to 21 years, while some reach the final stage in 4-5 years. 


Exercise and intellectual stimulation reduce risk, while high blood plresure, high cholesterol, diabetes, and blood vessel damage increse risk.  Ramdomized trials have generally confounded conclusions of crossectional analysis.  Aspirin has been shown to reduce risk. 


 Those who are trisomy for 21 (Down syndrome) almost universally exhibit AD by the age of 40. 


Neuroligical examination of early AD differentiates it sometimes from other conditions.  SPECT proves best.  Another recent objective marker of the disease is the analysis of cerebrospinal fluid for β amyloid or tau proteins. 


Drug therapies provide modest improvement at best.  They are used to treat symptoms and do not effect the course of the disease, and such symptomatic benefits are minimal at best.  There is some question as to the effectiveness of cholinesterase inhibitors. A number of recent articles have criticized the design of studies reporting benefit from these drugs, Because of their manyh side effects and their cost, they have doubtful clinical utility.  NMDA antagonists (a recent development) have shown some clinical efficacy.  The statin simvastatin has been found to reduce the incidence of Alzheimer's disease and Parkinsons disease by almost 50% in one study.  Possible an immunotherapy via vaccine will prove safe.  Clinical trials of one were stopped because of symptoms resembling menigoencephalitis; however, 20% of those so treated developoed high levels of antibodies to βA and showed sloer progression of AD.   


The term AD was not used independently of early onset until 1977 following a conference.   


The ability of SPECTROPHOTOGRAPY to differentiate the vascular cases from Alzheimer disease has not been established.  Too often mental decline caused by drugs such as statins, hypertension drugs, and psychiatric drugs--to name the main one--is diagnosed as AD. This is made more common by the incentives to treat AD. 


Vascualr Dementia

Because of tobacco smoke being the major cause of athereosclorsis, it is the major cause of this type of dementia.  A through evaluation for strokes should be done.  CT and MRI may show bilateral multiple infarcts in the dominant hemisphere and limbic structure, multiple lacunar strokes, or periventricular white-matter lesions extending into the deep white matter. 


The 5-year mortality rate is 61%, which is higher than AD because of artherosclerotic disorders coexisting.  Progression may be slowed by cholesterol-lowering therapy, regulation of blood sugar, and smoking cessation. 


Other Dimentias include Lewy Body and HIV-associated, alcohol associated, and frontotemporal.  FTD accounts for up to 10% of all dimentias.  Its typical onset is 55-65.  FTD is characterized by severe atropy, neuronal loss, gliosis, and adnormal neurons (Pick cells).  About of FTD is inherited

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