HomeresearchParkinson's and brain degeneration - prostate medication helpful

Parkinson’s and brain degeneration – prostate medication helpful


Terazosin (Vicard®) is an alpha receptor activator that increases blood flow to the prostate. As a side effect, a significant improvement in ATP production (energy) in the brain was now found. This was noticed because Parkinson’s patients with prostate problems and Vicard medication had much better outcomes. Preclinical studies of terazosin in Parkinson’s disease were successful.

Maybe this drug can even be used in degenerative disorders to improve blood circulation?

We would then have Trazodone (Trittico®) as another repurposed drug for causal treatment of neurodegenerative diseases


only 700 studies in Google Scholar on this Topic, all brand new and successful across the board!

Here 2 typical studies translated and summarized


A pilot project to assess the target effect of terazosin in Parkinson’s disease

Study 2022

Summary by Dr. Retzek

It happened by chance that Parkinson’s patients who received terazosin as a prostate medication had a much better outcome – while tamsulosin patients had increased rates of Parkinson’s and Alzheimer’s disease.

A randomized double-blind study with Parkinson’s patients taking terazosin is being carried out (highest level of validity) to see that the known in vitro effect of terazosin: the increase of ATP in the nerve cells is actually present in vivo.

Side effects were a reduction in blood pressure due to the expansion of blood vessels (dizziness).

Result: much more ENERGY was detected in the brains of affected patients, and the ATP content was also increased directly in the blood

Conclusion: it actually works, you get a direct causal therapy – unlike L-Dopa which is only symptomatic!


Orginal abstract of the study in German translation


Impaired energy metabolism in the brain is a key feature of Parkinson’s disease (PD). Terazosin (TZ) binds phosphoglycerate kinase 1 and stimulates its activity, which promotes glycolysis and increases ATP levels.

Preclinical and epidemiological data suggest that TZ may be neuroprotective in Parkinson’s disease

Our aim was to evaluate the targeted engagement and safety of TZ in people with Parkinson’s disease.


We conducted a 12-week pilot study in people with Parkinson’s disease. Participants were randomized to receive 5 mg TZ or placebo. Participants and study staff were blinded. We assessed TZ target engagement by measuring brain ATP with 31P magnetic resonance spectroscopy (MRS) and whole blood ATP with a luminescence assay. Robust linear regression models compared changes between groups controlling for baseline brain and blood ATP levels, respectively. We also assessed clinical measures of Parkinson’s disease and adverse events.


Thirteen participants were randomized. Mild dizziness/dizziness was more common in the TZ group, and three participants taking TZ discontinued treatment due to dizziness and/or orthostatic hypotension. Compared to the placebo group, there was a significant increase in the ratio of ATP to inorganic phosphate in the brain in the TZ group. The TZ group also had a significant increase in ATP blood levels compared to the placebo group (p < 0.01).


This pilot study suggests that TZ could achieve its goal and alter ATP levels in the brain and blood of people with Parkinson’s. Further studies may be required to test the disease-modifying potential of TZ.


Second study – Tamsulosin increases the risk of Parkinson’s, terazosin improves it

Tamsulosin =  Alna retard®,  Aglandin®, Tamsu®, Dutaglandin®,

my summary

Terazosin improves mitochondria in Parkinson’s patients. Studies show that taking the drug (for the prostate or heart) reduces the risk of Parkinson’s disease compared to tamsulosin users.

Meanwhile I found another study that describes

t that tamsulosin also increases Alzheimer’s dementia

Almost 115,000 patients are now being examined here, Parkinson’s occurs in 1.5% of the tamsulosin patients, only in 1% of the terazosin patients as well as in 1% of the “control patients”.

Conclusion: Terazosin and similar agents do not increase the risk of Parkinson’s disease, but neither do they reduce it compared to the control group. Tamsulosin patients have a minimal risk increase of 0.5% (I would ignore that).

here is the study from 2021

Study abstract in German translation

Parkinson’s disease in patients treated with α1-adrenergic receptor antagonists for benign prostatic hyperplasia

BACKGROUND. Recently, the α1-adrenergic receptor antagonist terazosin was shown to activate PGK1, a possible target for the mitochondrial deficits in Parkinson’s disease, which are related to its function as an initial enzyme in ATP synthesis during glycolysis. An epidemiological study of terazosin users showed a lower incidence of Parkinson’s disease compared to users of tamsulosin, a different class of α1-adrenergic receptor antagonist that does not activate PGK1. However, previous research on tamsulosin suggests that it may actually increase neurodegeneration, raising questions about whether it is an appropriate control group.

METHODS. To answer this question, we conducted an epidemiological study of the incidence of Parkinson’s disease in 113,450 individuals from the United States with a follow-up of 5 or more years. Patients were divided into tamsulosin users (n = 45,380), terazosin/alfuzosin/doxazosin users (n = 22,690), or controls matched for age, sex, and Charlson comorbidity index score (n = 45,380).

RESULTS. The incidence of Parkinson’s disease in tamsulosin users was 1.53%, significantly higher than in both terazosin/alfuzosin/doxazosin users (1.10%, P < 0.0001) and matched controls ( 1.01%, P < 0.0001). Terazosin/alfuzosin/doxazosin users did not differ in Parkinson’s risk from comparable controls (P = 0.29).

DIPLOMA. These results suggest that zosins may not have a protective effect against Parkinson’s disease, but that tamsulosin may in some way increase the progression of Parkinson’s disease.