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Clinical disorder
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Alzheimer
Neurological deterioration of cognitive functions usually on elderly
 Neural compartmental intracell (6)
  
SN Neuron CF-Compartment Intracellular element URL Query String
1 Hippocampus CA1 pyramidal cell Soma
2 Hippocampus CA1 pyramidal cell Soma
3 Dentate gyrus granule cell Soma
4 Neocortex V1 pyramidal corticothalamic cell Soma
5 Neocortex V1 pyramidal intratelencephalic cell Soma
6 Olfactory bulb main mitral cell Soma
 Neural compartmental extracell (7)
  
SN Ion channel Receptor(s) Neuron CF-Compartment Extracellular element References/notes URL Query String
1 I A Hippocampus CA1 pyramidal cell Soma Application of beta-amyloid to outside-out patches reduces the A-current; leading to increased dendritic calcium influx and loss of calcium homeostasis, potentially causing synaptic failure and initiating neuronal degenerative proceses(Chen C 2005).
2 I A Hippocampus CA1 pyramidal cell Middle oblique dendrite A model shows that block of I_A is sufficient to cause membrane depolarization, calcium influx, and increased excitability (Good TA, Murphy RM 1996).
3 I L high threshold Hippocampus CA1 pyramidal cell Middle oblique dendrite "The toxicity of beta-Amyloid(25-35) implicates a potentiation of L-type Ca currents ..." (Rovira C, et al. 2002).
4 I Calcium NMDA Hippocampus CA1 pyramidal cell Distal apical dendrite Impairment of LTP by beta-Amyloid is independent of NMDA receptors or voltage dependent Ca currents (Nomura I et al. 2005)
5 Hippocampus CA1 pyramidal cell Middle oblique dendrite "The effect of intracerebroventricular (icv) injections of beta-amyloid peptide fragments Abeta[15-25], Abeta[25-35], and Abeta[35-25] were examined on synaptic transmission and long-term potentiation (LTP) in the hippocampal CA1 region in vivo. ... LTP was, however, markedly reduced by Abeta[25-35; 10 nmol] (129 +/- 9%, n = 6, P < 0.001) and blocked by Abeta[25-35; 100 nmol] (99 +/- 6%, n = 6, P < 0.001). ... The Abeta-peptides tested were also shown to have no significant effect on paired pulse facilitation (interstimulus interval of 50 ms), suggesting that neither presynaptic transmitter release or activity of interneurons in vivo are affected. The effects of Abeta on LTP are therefore likely to be mediated via a postsynaptic mechanism. This in vivo model of LTP is extremely sensitive to Abeta-peptides that can impair LTP in a time- ([25-35]) and concentration-dependent manner ([25-35] and [35-25]). These effects of Abeta-peptides may then contribute to the cognitive deficits associated with Alzheimer's disease." (Freir DB et al. 2001)
6 I Calcium Hippocampus CA1 pyramidal cell Middle oblique dendrite "...beta-Amyloid(1-40) is related to an increase of non-L-type Ca channels ..." (Rovira C, et al. 2002).
7 NMDA Hippocampus CA1 pyramidal cell Distal apical dendrite a fragment of a protein that is snipped from amyloid precursor protein Impairment of LTP by beta-Amyloid is independent of NMDA receptors or voltage dependent Ca currents (>547<).
Other categories referring to Alzheimer
Pathological mechanism.Pathology   (82)
Neural compartmental extracell.Affected in disease   (7)
Neural compartmental intracell.Affected in disease   (6)
Revisions: 2
Last Time: 6/22/2006 1:16:01 PM
Reviewer: System Administrator
Owner: System Administrator