The researcher says that zinc imbalances in the brains of patients with Alzheimer's disease indicate new therapies

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Alzheimer's disease steals memory and destroys lives. Despite almost daily reports of promising new therapies, Alzheimer's disease remains undiagnosed. Now a new study reveals the mechanism by which Alzheimer's disease can cause memory loss and proposes new therapies.
Zinc and

The Alzheimer's disease brain has two types of lesions: beta-amyloid plaques on the outside of neurons and neurofibrillary tangles inside them. Known Alzheimer's disease genes are associated with plaques, but Alzheimer's disease symptoms are associated with tangles that are composed of the "tau" protein, which is normally followed by microtubules. Excess beta-amyloid plaques trigger entanglement, disrupt microtubules, and cause memory loss, even with normal synaptic function. But how?

In the March 23 issue of PLoS One, researchers from Harvard, Boston University, Albert University, the University of Arizona and the Chopra Foundation report that Alzheimer's disease memory loss is impaired by microtubules due to zinc imbalance.

Earder, Dr. Harvard's Rudolph Tanzi, the lead author of the current study, showed colleagues that plaques on the outside of neurons absorb traces and lower levels in neurons. Zinc strengthens many protein complexes, including microtubules (MT), tubulin polymers. MTs regulate synapses and play new publicly important roles in encoding neuronal memory.

In this study, Craddock et al identified 1) specific zinc-tubulin binding sites that promote tubulin interactions critical for MT polymer structure, 2) demonstrated by kinetic analysis how non-neuronal zinc sequestration intraneuronal zinc decreases available. to tubulin, can destroy MT and lead to entanglement. A 3) presented metallomics image mass spectrometry (MIMS) in mice with AD, which revealed an abnormal distribution of zinc in critical areas of the brain.

This view of Alzheimer's disease suggests therapies based on enhancing MT 1) by normalizing intraneuronal zinc levels with zinc ionophore drugs such as PBT2 (Prana Biotechnology), and 2) by stimulating MT self-organization and potency with other drugs such as transcranial therapies. , for example, ultrasound at MT resonant frequency in megahertz.

Tanzi, lead author and leading Alzheimer's specialist at Harvard, said: "Beta-amyloid plaques alone do not appear to be directly harmful, but lead to lower levels of zinc in neurons. This in turn disrupts the microtubules and ropes, causing entanglement and memory loss. Protecting microtubules and their association with tau may be the best way to treat Alzheimer's disease.

Article source: Citation: Craddock TJA, Tuszynski JA, Chopra D, Casey N, Goldstein LE, Hameroff SR, Tanzi RE (2012) The Zinc Dyshomeostasis Hypothesis of Alzheimer's Disease. PLoS ONE 7(3): e33552. doi:10.1371/journal.pone.0033552

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