We are analyzing https://link.springer.com/article/10.1007/s00401-009-0536-x.

Title:
Synaptic degeneration in Alzheimer’s disease | Acta Neuropathologica
Description:
Synaptic loss is the major neurobiological substrate of cognitive dysfunction in Alzheimer’s disease (AD). Synaptic failure is an early event in the pathogenesis that is clearly detectable already in patients with mild cognitive impairment (MCI), a prodromal state of AD. It progresses during the course of AD and in most early stages involves mechanisms of compensation before reaching a stage of decompensated function. This dynamic process from an initially reversible functionally responsive stage of down-regulation of synaptic function to stages irreversibly associated with degeneration might be related to a disturbance of structural brain self-organization and involves morphoregulatory molecules such as the amyloid precursor protein. Further, recent evidence suggests a role for diffusible oligomers of amyloid β in synaptic dysfunction. To form synaptic connections and to continuously re-shape them in a process of ongoing structural adaptation, neurons must permanently withdraw from the cell cycle. Previously, we formulated the hypothesis that differentiated neurons after having withdrawn from the cell cycle are able to use molecular mechanisms primarily developed to control proliferation alternatively to control synaptic plasticity. The existence of these alternative effector pathways within neurons might put them at risk of erroneously converting signals derived from plastic synaptic changes into the program of cell cycle activation, which subsequently leads to cell death. The molecular mechanisms involved in cell cycle activation might, thus, link aberrant synaptic changes to cell death.
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Keywords {🔍}

google, scholar, pubmed, cas, disease, alzheimers, synaptic, protein, precursor, amyloid, neurosci, alzheimer, brain, neurol, dementia, aging, plasticity, expression, arendt, betaamyloid, loss, neuropathol, mice, exp, cell, neurobiol, masliah, neurons, cortical, hippocampal, human, pathology, article, cognitive, res, cortex, proteins, mechanisms, synapse, neuroscience, hansen, beta, terry, neuronal, memory, normal, dysfunction, impairment, related, hippocampus,

Topics {✒️}

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Questions {❓}

Davidsson P, Jahn R, Bergquist J, Ekman R, Blennow K (1996) Synaptotagmin, a synaptic vesicle protein, is present in human cerebrospinal fluid: a new biochemical marker for synaptic pathology in Alzheimer disease?
Götz J, Ittner LM, Kins S (2006) Do axonal defects in tau and amyloid precursor protein transgenic animals model axonopathy in Alzheimer’s disease?
Rabl-Rückhard (1890) Sind die Ganglienzellen amöboid?
Vincent I, Rosado M, Davies P (1996) Mitotic mechanisms in Alzheimer’s disease?

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