M2OVE—AD: Molecular Mechanisms of the Vascular Etiology of Alzheimer’s Disease

M2OVE—AD: Molecular Mechanisms of the Vascular Etiology of Alzheimer’s Disease

NIH is launching a new consortium exploring the vascular mechanisms
involved in Alzheimer’s disease. It’s called M2OVE-AD — Molecular Mechanism of the Vascular Etiology of Alzheimer’s disease. So, we have known for many years that Alzheimer’s disease patients—in addition to carrying lesions such as amyloid
plaques and tangles— very frequently harbor cerebral vascular lesions. We also have evidence suggesting that
maintaining vascular health can positively impact or delay the onset of a number of
neurodegenerative diseases. So, that’s where M2OVE-AD comes in, we’re trying
to actually understand the molecular networks that tie the many factors of
genetic and environmental vascular risks to processes known to initiate and
propagate Alzheimer’s disease. So, the science of M2OVE-AD is heavily rooted
in the exploration of molecular mechanisms by which genetic vascular risk factors
such as APOe4 or mid-life vascular risk factors such as type 2 diabetes or
hypertension or cardiovascular risks impact Alzheimer’s disease pathogenesis. And the
way by which we’re going about it is actually collecting many layers of
molecular data in subjects who participate in several epidemiologic
research studies supported by the National Institutes of Health. Currently, four multi-institutional academic groups constitute the M2OVE-AD Consortium, and what these teams will do is generate many layers of
molecular data collected post-mortem brains from Alzheimer’s disease patients
or ante-mortem in peripheral systems of subjects who are still living and
participate in several epidemiological studies Once the data is collected, they will apply cutting-edge analytical methods
to generate mathematical projections related to how the molecular networks
associated with various types of vascular risks are connected to various
disease traits—whether it be neuroimaging pathologic traits or cognitive traits. So, these predictions
will then be tested in a variety of animal models where various aspects of
vascular physiology or AD pathogenesis can be explored at a very detailed mechanistic
level. Each of the teams that participate in the M2OVE-AD Consortium
are already bringing together basic researchers, clinicians, translational
scientists, computational biologists; but in addition we felt that instead of
leaving these four teams to work separately on something that is
tremendously complex and will generate tremendously rich and complex data, that
we would bring them together to make sure that the discoveries that each team
makes can be rapidly replicated and validated within the four teams and
also to make sure that the data that is being generated within the consortium is
rapidly and broadly shared with the scientific community at large to allow
for a parallel analysis of the findings. The ultimate goal of M2OVE AD is threefold, the first is to contribute to the development of a
much better predictive model of Alzheimer’s disease that reflects its
heterogeneity and multifactorial etiology. The second is to discover and
characterize new therapeutic targets that could be tractable for disease
prevention, whether it be through pharmacologic or non-pharmacologic means. And the third goal is to identify molecular signatures that can be collected non-invasively measured in peripheral fluids and can be used to stratify patients for their entry
into clinical trials testing various novel therapeutics. This is critical if
we want to attain the goal of precision medicine for Alzheimer’s disease which
is to treat the right patient with the right drug at the right stage of the
disease M2OVE-AD is a joint venture of the National Institute
on Aging and the National Institute of Neurological
Disorders and Stroke.

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About the Author: Oren Garnes

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