Key points in our paper are:-
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.
• Researchers have identified mitochondrial dysfunction and brain
insulin resistance as early indicators of Alzheimer’s disease.
• 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.
• The cerebrospinal fluid of Alzheimer’s brains is deficient in fats and
cholesterol.
• Advanced glycation end-products (AGEs) are present in significant
amounts in Alzheimer’s brains.
• Fructose, an increasingly pervasive sweetening agent, is ten times as
reactive as glucose in inducing AGEs.
• Astrocytes play an important role in providing fat and cholesterol to
neurons.
• Glycation damage interferes with the LDL-mediated delivery of fats
and cholesterol to astrocytes, and therefore, indirectly, to neurons.
• ApoE induces synthesis of Aβ when lipid supply is deficient.
• Aβ redirects neuron metabolism towards other substrates besides
glucose, by interferingwith glucose and oxygen supply and increasing
bioavailability of lactate and ketone bodies.
• Synthesis of the neurotransmitter, glutamate, is increased when
cholesterol is deficient, and glutamate is a potent oxidizing agent.
• 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.
• Once sufficiently many neurons are destroyed, cognitive decline is
manifested.
• Simple dietary modification, towards fewer highly-processed
carbohydrates and relatively more fats and cholesterol, is likely a
protective measure against Alzheimer’s disease.
Liz & Glyn Wainwright 