AD patients were found

to be more impaired on higher-order olfactory tasks involving specific cognitive processes.57 Odor identification and recognition tests can be easily implemented in cognitive test batteries to detect already subclinical cases of AD. The impairment of smell recognition is of clinical importance, as patients often report malodorous sensations and changes in, eg, the taste of foods leading to behavioral alterations. Consequences may range from increasing malnutriton to the Inhibitors,research,lifescience,medical development of delusions of poisoning that may trigger aggressive behavior. The deterioration of the neural network in the entorhinal cortex leads to an impairment in the ability to store and retrieve different representations of smell, with the decaying network yielding increasingly “default Inhibitors,research,lifescience,medical values” that have the tendency to be of rather unpleasant character. This feature of the neural network of smell memory reflects the evolutionary pressure towards the secure recognition of “bad” smells pointing to poisonous or rotten food that is pivotal for the survival of the organism. AD and epileptic activity The selleck screening library incidence of unprovoked seizures is clearly higher in sporadic AD than in reference populations with implications for memory functions. Nonconvulsive epileptiform activity could underlie at least some of the cognitive impairments observed in AD. Up to 1 in 5 patients with sporadic Inhibitors,research,lifescience,medical AD has at least 1 unprovoked

clinically apparent seizure during their illness, Inhibitors,research,lifescience,medical and clinical guidelines recommend obligatory treatment for this condition. The risk of epileptic activity is greater in early-onset AD. Many mutations in the presenilin-1 gene are associated with epilepsy. Trisomy-21 patients with early-onset AD also have frank seizures in 84% of cases. Many Inhibitors,research,lifescience,medical patients with AD show fluctuations in cognitive functions such as transient episodes of amnestic wandering

or disorientation. While an intermittent inability to retrieve memories cannot be easily explained by relatively protracted processes such as neuronal loss, plaque deposition, or tangle formation, an abnormal epileptic activity of neuronal networks can. Extensive work in this Unoprostone field was published by the group of Lennart Mucke. They see the possibility that high levels of β-amyloid induce epileptiform activity, which triggers compensatory inhibitory responses to counteract overexcitation that lead to changes in synaptic circuitry and an increase in inhibitory activity in, eg, the temporal cortex. This leads to changes in the texture of the neural networks involved and might explain disruptions of the networks as seen in the default mode network (DMN) in AD.58-60 Transynaptic progression of toxicity effects of β-amyloid inducing epileptic activity from the entorhinal cortex to other brain regions may explain cognitive dysfunctions in AD.61 The default mode network AD affects the default mode network (DMN).