In Alzheimer’s disease (AD), angiotensin II receptor blockers (ARBs) could reduce cerebrovascular dysfunction, while angiotensin-converting enzyme inhibitors (ACEis) might increase brain amyloid-β by suppressing effects of the angiotensin-converting enzyme 1, an amyloid-β-degrading enzyme. However, ACEis could benefit patients with AD by reducing the amyloidogenic processing of the amyloid precursor protein, by central cholinergic and anti-inflammatory mechanisms, and by peripheral modulation of glucose homeostasis. We aimed to investigate whether the ACE insertion/deletion polymorphism is associated with clinical changes in patients with AD, while considering apolipoprotein E (APOE)-ϵ4 carrier status and blood pressure response to angiotensin modulators.

Consecutive outpatients with late-onset AD were screened with cognitive tests and anthropometric measurements, while their caregivers were queried for functional and caregiver burden scores. Prospective pharmacogenetic associations were estimated for 1 year, taking APOE-ϵ4 carrier status and genotypes of the ACE insertion/deletion polymorphism into account, along with treatment with ACEis or ARBs.

For 193 patients (67.4% women, 53.4% APOE-ϵ4 carriers), the ACE insertion/deletion polymorphism was in Hardy–Weinberg equilibrium (p = 0.281), while arterial hypertension was prevalent in 80.3% (n = 124 used an ACEi, n = 21 used an ARB). ARBs benefitted mostly APOE-ϵ4 carriers concerning caregiver burden variations, cognitive and functional decline. ACEis benefitted APOE-ϵ4 non-carriers concerning cognitive and functional decline due to improved blood pressure control in addition to possible central mechanisms. The ACE insertion/deletion polymorphism led to variable response to angiotensin modulators concerning neurological outcomes and blood pressure variations.

Angiotensin modulators may be disease-modifiers in AD, while genetic stratification of samples is recommended in clinical studies.

Suicide prevention for major depressive disorder (MDD) is a worldwide challenge, especially for suicide attempt (SA). Viewing suicide as a state rather than a lifetime event provided new perspectives on suicide research.

This study aimed to verify and complement SAs biomarkers of MDD with a recent SA sample.

This study included 189 participants (60 healthy controls; 47 MDD patients with non-suicide (MDD-NSs), 40 MDD patients with suicide ideation (MDD-SIs) and 42 MDD patients with SA (MDD-SAs)). MDD patients with an acute SA time was determined to be within 1 week since the last SA. SUICIDALITY Part in MINI was applied to evaluate suicidality. Absolute powers in 14 frequency bands were extracted from subject’s resting-state electroencephalography data and compared within four groups. The relationship among suicidality, the number of SA and powers in significant frequency bands were investigated.

MDD-SIs had increased powers in delta, theta, alpha and beta band on the right frontocentral channels compared to MDD-NSs, while MDD-SAs had decreased powers in delta, beta and gamma bands on widely the right frontocentral and parietooccipital channels compared to MDD-SIs. Beta 1 power was the lowest in MDD-SAs and was modulated by the number of SA. The correlation between suicidality and beta 1 power was negative in MDD-SAs and positive in MDD-SIs.

Reduced beta 1 (12–15 Hz) power could be essential in promoting suicidal behaviour in MDD. Research on recent SA samples contributes to a better understanding of suicide mechanisms and preventing suicidal behaviour in MDD.