Benzodiazepines Like Xanax/Ativan Are Neuroprotective Against Alzheimer's (Human MRI Study)

[Clyde]

Benzodiazepine use and neuroimaging markers of Alzheimer's disease in nondemented older individuals: an MRI and 18F Florbetapir PET study in the MEMENTO cohort - PubMed

Recent evidence suggests an association between benzodiazepines (BZDs) use and lower brain amyloid load, a hallmark of AD pathophysiology. Other AD-related markers include hippocampal atrophy, but the effect of BZDs on hippocampal volume remains unclear. We aimed at 1) replicating findings on...

pubmed.ncbi.nlm.nih.gov

In conclusion, our results suggest neuroprotective effects of BZDs and support the involvement of the GABAergic system as a potential target for blocking brain amyloid accumulation and hippocampal atrophy, possibly via reduction in neuronal activity and neuroinflammation. However, we do not intend to suggest that BZDs should be used to prevent AD because the chronic use of BZDs has several side effects, including increased risk of fall, dependence and cognitive impairment (attention, memory and executive impairments mostly, at least during the time they are being taken) that certainly overcome the potential benefits on neurodegeneration. It is worth reminding that guidelines for BZD prescription include a short duration of use, which may not exceed 1 month as a hypnotic and 3 months as an anxiolytic. Moreover, blocking amyloid pathology and hippocampal atrophy does not necessarily lead to a decreased incidence of AD, which involves multiple other pathophysiological mechanisms, such as tau pathology and vascular disorders. Nevertheless, our paper suggests that further investigations of GABA and/or TSPO related mechanisms involved in neuronal excitability and neuroinflammation may allow the identification of novel pathophysiological pathways in AD and provide pharmacological targets to reduce amyloid formation and hippocampal atrophy.

This snip from the paper's introduction should blow some minds because their finding is nothing new:

While epidemiological studies appear inconsistent, findings on a potential neuroprotective effect of BZDs appear more robust, especially in preclinical studies in which the use of BZDs was associated with neuroprotective effects as shown by lower amyloid deposition [5–7] and lower hippocampal cell death in mice [6], these two processes being considered hallmarks of the pathophysiology of AD. Moreover, two recently published neuroimaging studies have consistently found that chronic use of BZDs was associated with lower amyloid deposition in human. Indeed, a first pilot study in the ADNI cohort found lower amyloid load as assessed with 18F Florbetapir positron emission tomography (PET) in 15 BZDs users compared to matched BZD nonusers [8]. More recently, our group, in which most of the authors of the present report were involved, published a second larger PET study based on the MAPT cohort, in which the 47 BZDs users exhibited lower amyloid load compared to the 221 BZDs nonusers [9]. Because only two studies on the impact of BZDs on brain changes are available in clinical population, the potential neuroprotective effect of BZDs remains to be investigated in humans, and replication studies are needed, while other markers of neurodegeneration, such as hippocampal volume, may also be investigated in addition to amyloid load.