There is currently no established therapy to treat or prevent Alzheimer's disease. The ketogenic diet supplies an alternative cerebral metabolic fuel, with potential neuroprotective effects. Our goal was to compare the effects of a modified Mediterranean-ketogenic diet (MMKD) and an American *

Stressful events frequently comprise both neutral and emotionally arousing information, yet the impact of stress on emotional and neutral events is still not fully understood. The hippocampus and frontal cortex have dense concentrations of receptors for stress hormones, such as cortisol, which at high levels can impair performance on hippocampally dependent memory tasks. Yet, the same stress hormones can facilitate memory for emotional information, which involves interactions between the hippocampus and amygdala. Here, we induced psychosocial stress prior to encoding and examined its long-term effects on memory for emotional and neutral episodes. The stress manipulation disrupted long-term memory for a neutral episode, but facilitated long-term memory for an equivalent emotional episode compared with a control condition. The stress manipulation also increased salivary cortisol, catecholamines as indicated by the presence of ␣-amylase, heart rate, and subjectively reported stress. Stressed subjects reported more false memories than nonstressed control subjects, and these false memories correlated positively with cortisol levels, providing evidence for a relationship between stress and false memory formation. Our results demonstrate that stress, when administered prior to encoding, produces different patterns of long-term remembering for neutral and emotional episodes. These differences likely emerge from differential actions of stress hormones on memory-relevant regions of the brain.Stress profoundly influences memory in humans and other species (Kim and Diamond 2002;Roozendaal 2002). This effect is in part due to activation of the hypothalamic-pituitary-adrenal (HPA) axis, which elicits a cascade of stress hormones and culminates in the release of glucocorticoids (GCs) from the adrenal cortex. Many of the brain regions important for memory (hippocampus, prefrontal cortex, amygdala) have dense concentrations of GC receptors (Lupien and Lepage 2001), and the function of these regions can be influenced by elevated stress hormones (de Quervain et al. 2003).Stress or GC treatment can either impair (de Quervain et al. 2000), or enhance (Buchanan and Lovallo 2001;Cahill et al. 2003;Putman et al. 2004) memory performance, depending on several modulatory factors. One such factor is memory stage (i.e., acquisition/encoding, consolidation, retrieval). Glucocorticoids, interacting with adrenergic activation in the basolateral amygdala and the hippocampus, appear to impair delayed memory retrieval, but enhance memory consolidation (Kuhlmann et al. 2005a,b;Buchanan et al. 2006; but, see Diamond et al. 2006 for an example of stress-induced consolidation impairment).The timing of the stress manipulation determines which stage of memory will be affected by cortisol elevations. For example, consolidation is tested by administering stress or cortisol treatment immediately after training, and then testing retrieval after a long delay (e.g., Cahill et al. 2003), whereas retrieval is targeted by allowing the memory to be acquired a...

The present experiment demonstrates that exposure to a significant psychological stressor (administered before watching a slide show) preserves or even enhances memory for emotional aspects of an event, and simultaneously disrupts memory for non-emotional aspects of the same event. Stress exposure also disrupted memory for information that was visually and thematically central to the event depicted in the slide show. Memory for peripheral information, on the other hand, was unaffected by stress. These results are consistent with theories invoking differential effects of stress on brain systems responsible for encoding and retrieving emotional memories (the amygdala) and non-emotional memories (e.g., the hippocampal formation), and inconsistent with the view that memories formed under high levels of stress are qualitatively the same as those formed under ordinary emotional circumstances. These data, which are also consistent with results obtained in a number of studies using animals and humans, have implications for the traumatic memory debate and theories regarding human memory.

We discuss the question of differentiation along the anterior-posterior longitudinal axis of the hippocampus. Data from a recent fMRI study are reanalyzed to determine whether activations in these hippocampal regions are affected by the nature of the information being accessed during a scanning session in which participants thought about episodes from their lives. Retrieving detailed spatial relational information preferentially activated the posterior hippocampus, whereas retrieving information about locales (or contexts) preferentially activated the anterior hippocampus. These data support the view that there is functional differentiation along the longitudinal axis in humans that matches what has been seen in rats, namely, that the posterior (dorsal) hippocampus is crucial for precise spatial behavior, and the anterior (ventral) hippocampus is crucial for context coding.

Background The immune response in Alzheimer’s disease (AD) involves activation of microglia which may remove β-amyloid. However, overproduction of inflammatory compounds may exacerbate neural damage in Alzheimer’s disease. AD pathology accumulates years before diagnosis, yet the extent to which neuroinflammation is involved in the earliest disease stages is unknown. Objective To determine whether neuroinflammation exacerbates neural damage in preclinical AD. Methods We utilized cerebrospinal fluid (CSF) and magnetic resonance imaging collected in 192 asymptomatic late-middle-aged adults (mean age=60.98 years). Neuroinflammatory markers chitinase-3-like protein 1 (YKL-40) and monocyte chemoattractant protein-1 (MCP-1) in CSF were utilized as markers of neuroinflammation. Neural cell damage was assessed using CSF neurofilament light chain protein (NFL), CSF total tau (T-Tau), and neural microstructure assessed with diffusion tensor imaging (DTI). With regard to AD pathology, CSF Aβ42 and tau phosphorylated at threonine 181 (P-Tau181) were used as markers of amyloid and tau pathology, respectively. We hypothesized that higher YKL-40 and MCP-1 in the presence of AD pathology would be associated with higher NFL, T-Tau, and altered microstructure on DTI. Results Neuroinflammation was associated with markers of neural damage. Higher CSF YKL-40 was associated with both higher CSF NFL and T-Tau. Inflammation interacted with AD pathology, such that greater MCP-1 and lower Aβ42 was associated with altered microstructure in bilateral frontal and right temporal lobe and that greater MCP-1 and greater P-Tau181 was associated with altered microstructure in precuneus. Conclusion Inflammation may play a role in neural damage in preclinical AD.