It is based on three concepts that emanate from human’s evolutionary history: (1) The grandmother- hypothesis (GMH), which explains human longevity due to an evolutionary advantage in reproduction by trans- generational transfer of acquired knowledge. Consequently it is argued that mental health at old- age must be the default pathway of humans’ genetic program and not development of AD. Cumulative evidence from a multitude of experimental and epidemiological studies indicate that behavioural and environmental risk factors, which impair productive AHN, result in reduced episodic memory performance and in reduced psychological resilience. This leads to avoidance of novelty, dysregulation of the hypothalamic–pituitary–adrenal (HPA)- axis and cortisol hypersecretion, which drives key pathogenic mechanisms of AD like the accumulation and oligomerization of synaptotoxic amyloid beta, chronic neuroinflammation and neuronal insulin resistance.

Consequently, the UTAD provides a rational strategy for the prevention of mental decline and a system- biological approach for the causal treatment of AD, which might even be curative if the systemic intervention is initiated early enough in the disease process. Hence an individualized system- biological treatment of patients with early AD is proposed as a test for the validity of UTAD and outlined in this review. Keywords: Unified theory Alzheimer’s disease (UTAD), Grandmother- hypothesis (GMH), Neuronal rejuvenation (NRJ), Adult hippocampal neurogenesis (AHN), Law of the minimum (LOM), Curative AD therapy, Causal AD prevention. Background. Alzheimer’s disease (AD) is characterized by impairment of hippocampal episodic memory performance followed by a progressive decline of cognitive and social capabilities.

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Since AD is the major cause of cognitive decline and no curative drug has been developed, research worldwide is intense and highly competitive. Epidemiological, biochemical, molecular, genetic and animal studies provide different entry points into the complex disease process, which led to different theories about the aetiology of AD. Starting with age as the main cause and primary risk factor, AD is being explained by the oligomeric amyloid beta (A. In fact, the thought that aging per se is the primary cause of AD is so deeply engrained in our thinking and appears in almost every introduction in any scientific paper about AD to be a compulsory statement, which is rarely challenged.

But as I will argue, not only are there a number of serious arguments challenging the “age- is- the- primary- cause- dogma”, ageing as the overarching cause also hinders the development of a “unified theory of AD” (UTAD), which incorporates all key findings including the long list of well- known environmental and behavioural risk factors, hence explaining the aetiology and pathogenesis of this debilitating disease. In fact, the lack of a UTAD continues to limit the development of effective preventive measures and a curative treatment to trial and error. Therapeutic interventions that focus on such singled out mechanisms continue to fail . In addition, prevention trials, which rather base their regimen on the correction of more or less arbitrarily selected risk factors than on a complete theory of AD, were so far also limited in their overall success . In contrast, the proposed UTAD overcomes our concept of age per se as the major cause for AD, and provides an encompassing explanation of the aetiology and pathogenesis of Alzheimer’s. It also allows proposing a number of required individual life changing interventions in order to prevent AD with high probability. In addition, the UTAD might provide the logical framework for a curative regimen, as will be outlined at the end of this review.

I would like to point out that I have termed the proposed theory “UTAD” because it presents a systemic neurobiological framework of how all currently known major behavioural, environmental or genetic risk factors individually or in combinations initiate or accelerate the AD process, despite certain caveats that apply for most if not all theories: Although I tried to be as comprehensive and exhaustive as possible in my search using key words like for instance “AD risk factor”, “factors inhibiting AHN” or “neuroinflammation” in the Pub. Med database of the National Center for Biotechnology Information, some minor risk factors might have been overlooked, it needs to be seen if they will verify or falsify the UTAD. The same goes for risk factors, which are already acting today but have not been identified yet, or which emanate from future individual lifestyle choices or cultural developments.

Conversely, in some categories of risk factors (e. It is my hope that once the principal concept of the UTAD is accepted, all risk factors that interfere with the neurobiological mechanisms, which, according to the UTAD, are at the centre of AD can be recognized and investigated more efficiently. Last but not least, behavioural risk factors in context of the UTAD might lead to discussions about free will or freedom of action, which would also go beyond the scope of this review. Aging is required but not causal for ADMeasurement of insulin resistance of the hippocampal/temporal lobe by positron emission tomography with 2- deoxy- 2- . One may conclude that the development of AD obviously requires time and, therefore, the logical consequence is that the risk of developing AD will increase with age. But correlation does not a priori equal causation.

In this case, for a disease requiring time to develop, age might simply be a precondition but not necessarily a cause. If age was indeed the cause of the disease, AD would not only be a natural outcome of human aging but the fight against AD would be a fight against human nature, which is highly difficult to win. But, fortunately, many lines of evidence disagree with this explanation (for example see . Particularly from a human’s life history point of view, if age per se was indeed the main causative risk factor, why was AD essentially unknown around the beginning of the last century?

According to a recent estimate, age would have caused approximately 3. USA alone, making the disease very common . But a textbook on neurology published in the late 1. AD- like pathology . And still in 1. 93. Alzheimer’s description of amyloid plaques and neurofibrillary tangles as hallmarks of AD brain pathology had not found their way in a comprehensive textbook of pathology . It may be proposed that, at that time, death as a consequence of AD was a very rare event.

AD prevalence was maybe similar rare as in Japan at the mid of last century. A recent study provided significant evidence that not age but rather certain lifestyle factors explain the sevenfold (!) increase in AD prevalence over the last half of the 2. This dramatic increase was strongly associated with a change from the traditional Japanese diet/lifestyle towards a Western one, which mainly took place between 1.

In particular, besides a large increase in alcohol intake, the consumption of meat and animal products rose by seven- and fourfold, respectively. Animal products and meat are known to increase the risk of AD because they contain compounds such as excess iron (which particularly enhances the risk for Apo. E4 carriers, as will be detailed below), advanced glycation end products (AGEs) and arachidonic acid that have been shown to increase oxidative stress and inflammation in the brain (which also will be detailed below).

The dietary changes paralleled the dramatic increase in AD prevalence for those people aged 6. Japan, which rose from a low 1 % in 1. This trend in disease prevalence can neither be explained by a change in life expectancy nor by a genetic drift. Such relatively short intervals are rather known for other behavioural diseases like e. Consequently they one reviewer of the study warns, “unless Japanese people return to the traditional Japanese diet, AD rates in Japan are unlikely to decrease” .

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