Posting this link to a free full text paper as I may forget it.
There is a useful section on the way curcumin helps prevent aggregation.
I think you also need to be aware that Alzheimer’s Disease Linked to Diabetes
Well I hope the next post is a little more constructive and helpful to people who come to this blog hoping to find some sensible evidence based suggestions that may enable them to delay the onset of Alzheimer's or other dementias.
Mercola has provided a link to his source of statistics and I while using the upper figures from the ranges provided isn't distorting them unduly. Bear in mind Mercola has had several previous run ins with the FDA and doesn't have many friends in consensus medical opinion so ALL his online statements HAVE to be checked by his legal team before he can write anything. Only AFTER they have been double checked to see if they would stand up to legal scrutiny is he permitted to post.
I think the one in four people being affected by Alzheimer's includes the relatives carer's and other close family. I'm sure everyone with an Alzheimer's relative is affected by that and the stress it imposes on the family and friends.
I think your claim that we are living longer healthier lives is mistaken. Sure we may at the moment be living longer but surely not healthier lives. I don't know how many people you know aged 70 but try asking how many medications they are taking and what side effects they are experiencing? Sure I know a lot of blokes my age with Prostate cancer and while they certainly are still alive it's not the same quality of life that they experienced before treatment. Try asking how many are on statins and what the side effects of those are and any reasonable person would question if the trade off between the claimed risk reduction and the actual side effects they are experiencing is actually worth it is certainly debatable. Early detection of many conditions now doesn't necessarily lead to any reduction in all cause mortality but certainly leads to increased medical costs, treatments and other iatrogenic consequences.
While it is true that 10% of Alzheimer's is attributed to genetic predisposition I think it would have been better if you had pointed out this is mainly through the maternal DNA so people whose fathers but not mothers had AD can ignore that potential risk factor. While it may be different in the USA, in the UK I'm not sure that most people appreciate that the genetic predisposition for AD is generally through the maternal side. While genes certainly load the gun it's still environmental/dietary factors that pull the trigger, so even if your mother did get AD and you have had your DNA checked and found you carried the risk that still does not mean there is absolutely nothing you could try to prevent or delay onset of AD.
You will have to apply a bit of common sense and have an element of luck but I think it's simply untrue to state that 90% of Alzheimer’s cases are sporadic, meaning the disease occurs for no apparent reason.
We know what the basic risk factors for AD are and we know roughly (though I accept not all the dots are as yet connected) how this impacts on disease initiation therefore I contend that most of the suggestions Mercola makes are sufficiently evidence based to be worthy of investing some time examining the evidence he uses and which are also supported by papers listed at Pubmed.
We have to take Alzheimer's incidence very seriously in the light of the explosion in obesity and diabetes. These conditions predispose people to increased risk of dementia so it shouldn't be hard to work out that AD incidence will inevitably also increase.
Therefore to do everything possible to reduce hyperglycaemia and conditions that result from raised levels of inflammation is simply common sense.
There was a recent report of a 68 yr old woman on being given an Alzheimer's diagnosis immediately walking in front of a train, irrespective of whether this was a direct result of knowing the diagnosis or just a consequence of the condition (obviously we'll never know) we should not give people the impression an Alzheimer's diagnosis is a fate worse than death and that pharmaceutical drugs are the only or even the best way of managing this dreadful condition. We ought be talking about The Myth of Alzheimer's, What You Aren't Being Told About Today's Most Dreaded Diagnosis Aging with Dignity; Aging with Hope
Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs.
Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression.
In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deﬁciency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease.
A ﬁrst step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport.
This leads to cholesterol deﬁciency in neurons, which signiﬁcantly impairs their ability to function.
Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis.
Other neurodegenerative diseases share many properties with Alzheimer's disease, and may also be due in large part to this same underlying cause
1. The amyloid-β present in Alzheimer's plaque may not be causal, since drug induced suppression of its synthesis led to further cognitive decline in the controlled studies performed so far.
2• Researchers have identiﬁed mitochondrial dysfunction and brain insulin resistance as early indicators of Alzheimer's disease.
3• ApoE-4 is a risk factor for Alzheimer's disease, and ApoE is involved in the transport of cholesterol and fats, which are essential for signal transduction and protection from oxidative damage.
4• The cerebrospinal ﬂuid of Alzheimer's brains is deﬁcient in fats and cholesterol.
5• Advanced glycation end-products (AGEs) are present in signiﬁcant amounts in Alzheimer's brains.
6• Fructose, an increasingly pervasive sweetening agent, is ten times as reactive as glucose in inducing AGEs.
7• Astrocytes play an important role in providing fat and cholesterol to neurons.
8• Glycation damage interferes with the LDL-mediated delivery of fats and cholesterol to astrocytes, and therefore, indirectly, to neurons.
9• ApoE induces synthesis of Aβ when lipid supply is deﬁcient.
10• Aβ redirects neuron metabolism towards other substrates besides glucose, by interfering with glucose and oxygen supply and increasing bioavailability of lactate and ketone bodies.
11• Synthesis of the neurotransmitter, glutamate, is increased when cholesterol is deﬁcient, and glutamate is a potent oxidizing agent.
12• Over time, neurons become severely damaged due to chronic exposure to glucose and oxidizing agents, and are programmed for apoptosis due to highly impaired function.
13• Once sufﬁciently many neurons are destroyed, cognitive decline is manifested.
14• Simple dietary modiﬁcation, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease.