Dissociation of Alzheimer's morphological pathology from cognitive impairment

We observed the Alzheimer's morphological pathology, amyloid production induces Alzheimer's cognitive impairment, was dissociated from the cognitive impairment. The earlier Alzheimer's pathological changes can be induced in normal C57BL mice, by B6 deficient feeding 4 months with no amyloid, and this cognitive and memory impairments were completely inhibited by anti-homocysteic acid antibody. According to Koch's postulate, if a pathogen of Alzheimer's disease is administrated to the normal animal, we would observe the Alzheimer's cognitive impairment in the normal animal. We actually have observed this cognitive impairment in normal C57BL male mice with no amyloid. From our observations, it is suggested the dissociation of Alzheimer's morphological pathology may be possible from the cognitive impairment

The Notebook: An Accidental Alzheimer\u27s Awareness Campaign

My paper examines and critiques the portrayal of Alzheimer¹s disease in the popular film, The Notebook. Based off of a Nicholas Sparks novel, The Notebook uses Alzheimer¹s disease as a vehicle to relay a love story, but in doing so, presents a distorted picture of Alzheimer¹s disease to its audience. My paper compares the responsibilities of family caregivers of Alzheimer¹s patients in today¹s world with the unrealistic family caregiver, Noah, depicted on screen. My paper also explores and exposes inconsistencies between the attractive nursing home experience presented on screen and the less than ideal treatment patients experience in long term care facilities in America today. In addition, my paper uses several other films to examine and compare the emotional distress Alzheimer¹s disease patients and their families face when confronted with the condition: further underlining the idealized familial encounter with the disease depicted in The Notebook. My paper also examines the glamorized representation of Alzheimer¹s disease symptoms in the film. The misrepresentation and glamorization of Alzheimer¹s disease in The Notebook elicit serious implications in today¹s society. My paper describes how Alzheimer¹s awareness groups and other organizations utilize The Notebook as an educational tool to raise awareness for the condition, despite its imperfections. For better or worse, in today¹s society, people absorb a myriad of information from film and pop culture, leaving filmmakers with the difficult task of balancing entertainment and medicine in their films. Ultimately, my paper highlights this imbalance in The Notebook and describes its resulting accidental Alzheimer¹s awareness campaign

Preventing the Unnecessary Losses of Alzheimer\u27s Disease

Educational Objectives 1. To state the importance of early detection and diagnosis of Alzheimer\u27s disease. 2. To describe common concerns of people in the early stages of Alzheimer\u27s disease. 3. To describe interventions to help people who have recently been diagnosed with Alzheimer\u27s disease or other dementias

Effects of cromakalim (BRL 34915) on potassium conductances in CA3 neurons of the guinea-pig hippocampus in vitro

The action of the potassium channel activator, cromakalim (BRL 34915), on membrane potential, input resistance and current-voltage-relationship of CA3 neurons in a slice preparation of the guinea-pig hippocampus was investigated by means of intracellular recordings. In the presence of tetrodotoxin, cromakalim (30–100 mol/l) produced a hyperpolarization up to 4 mV associated with a decrease in input resistance up to 10 MOhms. Determination of the equilibrium potential of the cromakalim action revealed that the hyperpolarization is due to the activation of a potassium conductance. This cromakalim-activated potassium conductance was voltage-dependent, i.e. it increased with hyperpolarization. Among a number of potassium channel blockers tested, only Cs+ (2 mmol/l) and Ba2+ (0.5 mmol/1) were able to inhibit the cromakalim-induced effects. Simultaneously, both cations suppressed the hyperpolarizing inward rectification (anomalous rectification) in these neurons, indicating that cromakalim activated or potentiated an inwardly rectifying potassium conductance. In addition, cromakalim slightly enhanced both amplitude and duration of afterhyperpolarizations following single calcium-dependent action potentials, suggesting that cromakalim might have a weak facilitatory effect on calcium-dependent potassium conductances

Transient and selective blockade of adenosine A1-receptors by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) causes sustained epileptiform activity in hippocampal CA3 neurons of guinea pigs

The effects of endogenously released adenosine on the excitability of hippocampal neurons were studied using the novel and highly selective adenosine A1-receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Extra- and intracellular recordings performed in area CA1 and CA3 of the guinea pig hippocampal slice preparation revealed that a transient suppression of an inhibitory purinergic tonus by DPCPX leads to sustained interictal-like epileptiform activity arising in area CA3. Once induced, the spontaneous burst discharges were apparently irreversible within the observation period, even after prolonged washout (2–3h) in normal solution. In contrast, the hyperpolarizing action of exogenous adenosine, which was substantially reduced by DPCPX, recovered within 30–60 min of drug washout, indicating that DPCPX was not irreversibly bound to the A1-receptor

Amanda Hazy Wins Outstanding Thesis Award for Spring 2015

Amanda Hazy wins the Outstanding Thesis Award for Spring 2015 for her thesis, “Gene Expression and Alzheimer\u27s Disease: Evaluation of Gene Expression Patterns in Brain and Blood for an Alzheimer\u27s Disease Mouse Model.

Psychosis in Azheimer\u27s Disease

Much of the basic science literature on Alzheimer\u27s Disease (AD) reflects ongoing research into pathophysiology and neuropathology. Yet, despite reports of the association between psychotic symptoms and Alzheimer\u27s disease, relatively little is known about why such symptoms develop in certain patients and not in others. Neuroimaging and genetic studies may provide greater understanding of this association and allow clinicians and researchers to prevent, predict and treat the onset of psychotic symptoms in the future. This paper will review the current literature on the topic of psychosis in Alzheimer\u27s disease and focus on current recommendations for interventions by clinicians and caregivers

Disinhibition of hippocampal CA3 neurons induced by suppression of an adenosine A1 receptor-mediated inhibitory tonus: Pre- and postsynaptic components

Intracellular recordings were performed on hippocampal CA3 neuronsin vitro to investigate the inhibitory tonus generated by endogenously produced adenosine in this brain region. Bath application of the highly selective adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine at concentrations up to 100 nM induced both spontaneous and stimulus-evoked epileptiform burst discharges. Once induced, the 1,3-dipropyl-8-cyclopentylxanthine-evoked epileptiform activity was apparently irreversible even after prolonged superfusion with drug-free solution. The blockade of glutamatergic excitatory synaptic transmission by preincubation of the slices with the amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (10 μM), but not with theN-methyl-d-aspartate receptor antagonistd-2-amino-5-phosphonovaleric acid (50/μM), prevented the induction of epileptiform activity by 1,3-dipropyl-8-cyclopentylxanthine. The generation of the burst discharges was independent of the membrane potential, and the amplitude of the slow component of the paroxysmal depolarization shift increased with hyperpolarization, indicating that the 1,3-dipropyl-8-cyclopentylxanthine-induced bursts were synaptically mediated events. Recordings from tetrodotoxin-treated CA3 neurons revealed a strong postsynaptic component of endogenous adenosinergic inhibition. Both 1,3-dipropyl-8-cyclopentylxanthine and the adenosine-degrading enzyme adenosine deaminase produced an apparently irreversible depolarization of the membrane potential by about 20 mV. Sometimes, this depolarization attained the threshold for the generation of putative calcium spikes, but no potential changes resembling paroxysmal depolarization shift-like events were observed