sodium-lactate and Alzheimer-Disease

Bilateral temporoparietal hypoperfusion is a characteristic single photon emission computed tomography (SPECT) finding in Alzheimer's disease (AD). Lactate is a metabolic vasodilator and is known to provoke increased cerebral blood flow (CBF) in healthy adults. This work investigated whether lactate, which is present in high concentrations in AD cerebrospinal fluid, affects AD-specific perfusion abnormalities. Twenty mild-to-moderately demented AD probands participated in the self-controlled study. The regional CBF was examined utilizing (99m)Tc-HMPAO SPECT after sodium lactate infusion (0.5 M, 5 mL/kg body weight) and 0.9% NaCl infusion, one on each of two separate days. Despite the vasodilatator effects of sodium lactate, AD rCBF patterns did not show increase in temporo-parietal regions after its infusion. AD-specific bi-temporo-parietal reduction in CBF was accompanied by further hypoperfusion in the parieto-occipital areas after the sodium lactate infusion in seven patients, while no CBF changes were observed in the case of the remaining 13 probands. The pattern of the CBF abnormalities was not correlated with the apolipoprotein E genotype. The decreased vascular responsiveness to sodium lactate reflects disturbed vasoregulatory processes in AD and it is unlikely that lactate would have any relevance in the treatment of AD-related cerebral hypoperfusion, but could be used to improve the value of perfusion SPECT in the diagnosis of AD.

Topics: Aged; Alzheimer Disease; Cerebral Cortex; Female; Humans; Infusions, Intravenous; Male; Sodium Lactate; Tomography, Emission-Computed, Single-Photon

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.

Topics: Aged; Alzheimer Disease; Brain; Cortical Synchronization; Electroencephalography; Female; Humans; Infusions, Intravenous; Likelihood Functions; Male; Scalp; Sodium Lactate; Vasodilator Agents

Monoamine oxidase type B (MAO-B) activity is elevated in certain neurological diseases such as Alzheimer's and Parkinson's disease with respect to age-matched controls; the cause of this elevation is unknown. The documented accumulation of aluminum in certain neurodegenerative diseases prompted us to test the effect of Al3+ on the activity of MAO-B in rat brain homogenate. Results showed that the metal ion significantly increased MAO-B enzymatic activity in a dose-dependent manner, yielding a K(M) of 5.69 microM compared with 34.45 microM in the absence of the metal ion. The Vmax of 45.34 micromol/min was unchanged in the presence of the metal ion.

Topics: Aluminum; Aluminum Compounds; Alzheimer Disease; Animals; Brain; Cell Extracts; Deamination; Dose-Response Relationship, Drug; Enzyme Activation; Kinetics; Lactates; Male; Monoamine Oxidase; Parkinson Disease; Phenethylamines; Rats; Rats, Wistar; Sodium Lactate; Thermodynamics