I am just wondering if there is any connection between neurodegenerative diseases such as Alzheimers and hypertension/hypotension or increased/decreased sympathetic output? Any ideas, references or documents would be appreciated?
The latest research evidenced impact of stress, causing cardiovascular disease, in my opinion including hypertension is presented here
Good luck !
A Culture–Brain Link: Negative Age Stereotypes Predict Alzheimer’s Disease Biomarkers.Levy, Becca R.; Ferrucci, Luigi; Zonderman, Alan B.; Slade, Martin D.; Troncoso, Juan; Resnick, Susan M.
Psychology and Aging, Dec 7 , 2015, No Pagination Specified. http://dx.doi.org/10.1037/pag0000062
Abstract
Although negative age stereotypes have been found to predict adverse outcomes among older individuals, it was unknown whether the influence of stereotypes extends to brain changes associated with Alzheimer’s disease. To consider this possibility, we drew on dementia-free participants, in the Baltimore Longitudinal Study of Aging, whose age stereotypes were assessed decades before yearly magnetic resonance images and brain autopsies were performed. Those holding more-negative age stereotypes earlier in life had significantly steeper hippocampal-volume loss and significantly greater accumulation of neurofibrillary tangles and amyloid plaques, adjusting for relevant covariates. These findings suggest a new pathway to identifying mechanisms and potential interventions related to the pathology of Alzheimer’s disease. (PsycINFO Database Record (c) 2015 APA, all rights reserved)
The Deadly Link Between Heart Disease and Alzheimer’s
wrote by By Edward R. Rosick, DO, MPH, DABHM
If the threat of a heart attack is not enough to compel Americans to trade in their cheeseburgers and recliners for salmon and exercise bikes, how about mounting evidence that cardiovascular disease may greatly increase one’s risk of developing mind-destroying Alzheimer’s disease?
As scientists delve further into the twin pathologies of cardiovascular disease and dementia, they are increasingly convinced that afflictions of the heart and brain share common triggers and biochemical characteristics, including inflammation, oxidative stress, and hypoxia, an oxygen deficit caused by impaired blood flow.
Fortunately, many nutritional and botanical agents that have shown great efficacy in preventing and treating cardiovascular disease also appear to work via several important mechanisms to preserve healthy cognitive function and ward off the crippling effects of Alzheimer’s and other forms of senile dementia.
In this article, we examine the growing evidence indicating that cardiovascular disease may greatly increase one’s likelihood of developing Alzheimer’s, as well as strategies you can adopt today to safeguard the health of your heart and your mind.
Twin Afflictions of Heart Disease and Alzheimer’s
The latest data show that more than 60 million Americans suffer from some form of heart disease, including coronary artery disease, congestive heart failure, and cardiac arrhythmias (abnormal rhythms of the heart). Coronary artery disease in particular affects more than 13 million Americans.1 Although heart disease traditionally has been thought of as a “man’s disease,” nearly half of the 600,000 Americans who will die from heart disease this year are women. With its alarming growth rate and lack of a cure, Alzheimer’s disease is poised to become one of the most insidious medical problems of the twenty-first century. This devastating neurological condition progressively destroys one’s memory and ability to think. Alzheimer’s now affects more than 5 million Americans, including one of eight Americans aged 65 or older and nearly half of those over the age of 85. Someone in the United States develops Alzheimer’s every 72 seconds, and according to current projections, by 2050 a new case of Alzheimer’s disease will emerge every 33 seconds.For more plz read at following link.
there are quite some evidences that indicates that when the emotional system is affected (hip-amy) that reflects to output brain regions controlling the autonomous system and therefore resulting in autonomic dysfunction and eventually associated cardiovascular diseases.
http://www.ncbi.nlm.nih.gov/pubmed/7732768
http://www.ncbi.nlm.nih.gov/pubmed/16945211
It is difficult to provide causality in such pathologies because the protocols are most intended to prove an association.
A multicenter study led by Christian Haass and Michael Ewers of Ludwig-Maximilians-Universitaet in Munich has identified a biomarker associated with the activation of an innate immune response to neural damage during early stages of Alzheimer's disease.
AD has many factors which contribute to the its clinical features, increase the probability of developing this particular form of senile dementia and biochemically mediated events that can increase the aggressiveness of it parthenogenesis. Etiologically speaking, AD is hetero-genetic, presents in several similar clinical presentations, with the exception of early onset, linked to a familial mutation in Apolipoprotein E4 genes. Cerebral amyloid angiopathy, (CAA) also relies upon Amyloid beta protein build up within the carotid arteries, among other blood vessels of variable size; and it can contribute to cognitive decline; usually resulting from a stroke. While it is amyloid beta build up characterized in this condition it is not identical to AD, based upon 2 major chemical features:
1.) The AB is distinct in its location.
2.) The AB has differing amino acid sequences leading to an altered conformation.
Heart attacks are thought to be sometimes contribute to CAA, or CAA like disorders. As far as AD itself, there is a moderate, but statistically significant increase in risk of AD from both heart attacks and strokes, due to potential ion leakage channels being formed, which can via their electrostatic attractions/repulsion and interactions with various macro-molecules (like the proteins; AB as an example) and cell membranes, where differential diffusion of ions are altered leading to neuronal bursting, leakage of cellular materials and in the case of AB to tau interactions via signal transduction cascades which leads to hyper-phosphorylation of tau the basic protein of mircrotubules responsible for normal cellular transport.
In order to understand how strokes and heart attacks can contribute AD or AD like pathologies, one must learn: molecular biology in detail, basics of biochemistry of signal transduction, ion affects in vivo, and basic pathology: anatomy and physiology.
Strokes specifically also lead to overly aggressive activation of innate and adaptive immune system via: MAC/complement and then various cytokines as well; a little immunology would not hurt here as well.
Please see Alzforum.org for the best free AD resource in the world.