Metabolic correction

This approach is based on the prominent aspect of Alzheimer’s disease, which is common for many other neurodegenerative diseases: energy deficit. It has first been noted for the case of insulin insufficiency in the brain of Alzheimer’s patients. Because of that Alzheimer’s disease has been called “Type 3 diabetes” [14] and the insulin modification therapies are in pharmaceutical’s pipelines.

Angiotensin receptor blockers

A retrospective analysis of five million patient records with the US Department of Veterans Affairs system found that different types of commonly used anti-hypertensive medications had very different AD outcomes. Those patients taking angiotensin receptor blockers (ARBs) were 35—40% less likely to develop AD than those using other anti-hypertensives.[17]

Antibiotic therapy

Only one clinical trial is being done (at McMaster University) to investigate the efficacy of antibiotic therapy.[18] The authors of the study indicated that it was effective in delaying the progress of the disease: “In conclusion, a 3-month course of doxycycline and rifampin reduced cognitive worsening at 6 months of follow-up in patients with mild to moderate AD.”[19] A re-examination of the same data using: “…AUC analysis of the pooled index showed significant treatment effect over the 12-month period”.[20]

Several studies using minocycline and doxycycline, in an animal model of Alzheimer’s Disease, have indicated that minocycline[21][22] and doxycycline[23][24] exerts a protective effect in preventing neuron death and slowing the onset of the disease.

Antiviral therapy

The possibility that AD could be treated with antiviral medication is suggested by a study showing colocation of herpes simplex virus with amyloid plaques.[25]


The endocannabinoid system may have a role in AD.[26][27] For instance, THC, one of the active ingredients in marijuana, has been show to reduce amyloid beta plaque formation through inhibition of acetylcholinesterase (AChE).[28


From gene expression patterns obtained in microarray datasets, correlation between cellular physiology and diseases can be revealed. Divergence studies (e.g. Jensen-Shannon divergence computations which interprets difference in gene expression and probability of distribution patterns) reveals gene expression distribution difference between AD and normal aging brains.[80] That is, expressed genes that are negatively correlated with normal aging brain but are positively correlated with AD brains are possible biomarkers for AD diagnosis and treatment. Combining KEGG and PATHWAY studio, ATP5C1, COX6A1, NDUFV2, PLCB1, and PPP3CA are metabolism and mitochondrial-related genes that have been shown to be reduced in AD samples.[81][82][83] Furthermore, metabolic dysregulations such as calcium homeostasis [84] and insulin signaling have also been identified to contribute to the onset of AD. Genes that are associated with calcium and insulin signaling are found using GATHER (online bioinformatics tool for analyzing genomic signatures).[80] In fact, insulin signaling impairment and AD has been considered to be related in many levels. Functional protein sequence alignments (e.g. ClustalW, MUSCLE) and phylogenetic analysis (e.g. Phylip, Mega) demonstrate that acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) are highly linked in these two diseases.[85] Increased BChE contributes altered lipoprotein metabolism and insulin insensitivity,[86] and is positively correlated to hypertension and diabetes in correlation studies.[87] AChE allows stabilization of neurotransmitter, acetylcholine (ACh), which is one of the main target for AD treatment. However, recent in silico pharmacological study examined drug-disease interaction showed that AChE inhibitors may not be the answer to AD treatment. PKC, ARG, HDAC, and GSK3 inhibitors that regulate calcium homeostasis and genetic modification of cell cycle and apoptosis may be the future targets of AD medication.[88]

Neuronal plasticity is a key player in cognitive function that cannot be ignored in study of AD progression. Microarray studies found that NEFM, NEFL, and SV2B are highly downregulated in samples obtained from severe AD patients. NEFL is a neurofilament gene that has been shown to be related to hypotrophy of axons in motorneurons when mutated.[89] However, both neurofilaments (NEFL and NEFM) have been documented to be involved in neurological disease, Charcot-Marie-Tooth,[90][91] instead of AD, which demonstrate possible unknown connections of AD to other neurological diseases. SV2B is another gene that is downregulated in AD and has been shown to be related to neurodegeneration, particularly synaptic calcium-regulated exocytosis.[92] The downregulation of genes responsible for neural synapse and neuroplasticity is related to another family of protein that has been found to be related to AD pathogenesis, EGR (early growth response).[93] This EGR is regulated by upregulated FOXO1 (Forkhead Box O1) through PI3K/Akt pathway,[94] which is listed as one of the pathway for future in anti-AD medication.[88] These findings using computational methods allow for the connection of different studies and facilitate the understanding of disease complexity as well as directing to new possible biomarkers of AD.


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