Altered platelet physiology

The appropriateness of using platelets, as a cell mirroring some neurochemical processes, finds its rationale in the numerous similar features of platelets and neurones Platelets store and release neurotransmitters and express appropriate neurotransmitter transporters and some neurone-related proteins such as NMDA receptors. Along these lines, different authors reported abnormalities in platelets physiology and function in AD. At first, Zubenko and colleagues described an alteration in platelet membrane fluidity in AD patients [99]. Other studies, performed on platelets obtained from patients with moderate to severe AD, reported cytoskeletal abnormalities, cytochrome oxidase deficiency, abnormal cytoplasmic calcium... 

Although this model was consistent with results obtained using A23187, which is known to alter intracellular cation gradients (18,19J, a similar mechanism of action by physiological platelet agonists, e.g. ADP, epinephrine, thrombin,... 

The work discussed here has shown that suspensions of platelets and red cells in a physiological medium can provide information for platelet surface interactions. Evidence is provided on the dynamic features of platelet-surface adhesion and detachment which indicates that more than one sequence of adhesion, detachment and re-adhesion can lead to the same net platelet adhesion. Surface generated substances, such as A DP and serotonin from platelets and thrombin from the coagulation pathway, may strongly influence the function of platelets approaching a surface. The supply of these substances depends on the presence of flow and continued arrival of platelets at a surface. The reactivity of surface-bound protein may be altered by platelet adhesion and detachment. This may occur as a result of deposition of cell membrane components, replacement of the original substrate with protein secreted from platelets or possibly by enzymatic digestion of surface bound protein. 

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