Background: A large body of studies characterized the renal and cardiovascular effects
of the peptides of the renin-angiotensin system (RAS). We now recognize that, in addition to angiotensin
(Ang) II and Ang III, other peptides, such as, Ang-(1-7), Ang-(1-9), Ang IV and Alamandine
can mediate actions of the RAS in different tissues, including the brain. Effects elicited by angiotensins
in the brain are complex, site specific and dependent on the interaction with selective receptors,
angiotensin type 1 receptor (AT1), AT2, Mas or MrgD, which present widespread distribution
in the central nervous system. Although the majority of studies indicate a neuroprotective action for
the inhibition of angiotensin converting enzyme or blockade of AT1 receptor, recent studies point to
the participation of other angiotensin peptides in the pathophysiology of the neurodegenerative
Objectives and Methods: In this article, we revised the literature to describe recent findings related
to the role of RAS in neurodegenerative diseases such as, Parkinson, Alzheimer, Huntington and
Results: The results obtained are promising and may stimulate the development of novel and more
effective pharmacological tools to prevent and better control neurodegenerative diseases. In this
brief review, we present results from studies showing the participation of the RAS with respect to
neurodegenerative diseases, such as, Parkinson, Alzheimer, Huntington and Multiple Sclerosis.
Conclusion: Increased RAS activity leading to increase in Ang II levels, may increase the risk of
developing PD, AD, HD or MS. However, the alteration in the balance among angiotensin peptides
resulting in increasing Ang-(1-7) or Alamandine may represent effective neuroprotective strategy in
population groups at high risk or as coadjutant treatment to reduce the progression of these diseases.
Although most studies suggest a neuroprotective action for ACE inhibition or AT1 receptor
antagonism, many studies will still be needed to characterize the relative importance (and intracellular
mechanisms) of each RAS peptide for the pathophysiology of neurodegenerative diseases. The
results to date are promising and may lead to new and more effective pharmacological tools to prevent
and better control neurodegenerative diseases.