Sodium lactate differently alters relative EEG power and functional connectivity in Alzheimer’s disease patients’ brain regions

Abstract

Bilateral temporo-parietal hypoperfusion and decreased glucose metabolism are characteristic in vivo findings in Alzheimer's disease (AD). Lactate is a metabolic vasodilator and is known to induce increased cerebral blood flow in healthy adults. The present study addresses the issue whether sodium lactate infusion affects functional state and resulting electroencephalographic patterns of AD patients. Twelve late-onset sporadic AD probands participated in this self-control study. The relative power and synchronization likelihood (SL) values of the electroencephalographic samples were calculated and compared off-line before and after sodium lactate infusion (0.5 M, 5 ml/kg body weight). Based on the reactivity to sodium lactate the scalp could be divided into three parts; no significant changes were seen in the seriously damaged (P3-P4) areas. The moderately affected regions in the close neighborhood showed a paradoxic inactivation with electroencephalographic slowing, a likely consequence of the metabolic-like steal effect of the near-normal areas outside. These results indicate a diminished vascular and/or metabolic reserve capacity to sodium lactate challenge in AD and confirm the formerly described electroencephalographic abnormalities.

Lactate infusion as therapeutical intervention: a scoping review

“…Sodium lactate has been infused to patients with diabetes mellitus [ 19 – 25 ], traumatic brain injury (TBI) [ 11 , 26 – 34 ], and Alzheimer’s disease [ 35 – 37 ].…”

“…Impaired cerebral microcirculation and glucose metabolism are established markers of Alzheimer’s disease. To our knowledge, three studies have investigated whether lactate could serve as an alternative energy source and positively influence cerebral blood flow in patients with Alzheimer’s disease [ 35 – 37 ]. Unfortunately, it did not seem to improve cognitive functioning of the patients.…”

Graph Theory and Brain Connectivity in Alzheimer’s Disease

“…Biomarkers for AD are being researched on a variety of different scopes such as biochemical (Bajo and others 2015; D’Amelio and Rossini 2012; Jardanhazy and others 2008), genetic (De Jager and others 2014; Hawrylycz and others 2015), neurophysiological, and neuroimaging (Kim and others 2015b). For a review on the differences between these methods, see Mirzaei and others (2016).…”

Might Cortical Hyper-Responsiveness in Aging Contribute to Alzheimer’s Disease?

“…Excito-toxicity could promote changes in the generation and processing of endogenous proteins that compose the plaques and tangles of AD [74]. This might further exacerbate network incoherence [75] and critically impair spectral power generation [76]. Thus, aging and AD are neurophysiologically distinguishable, and their association may be causal.…”