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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Alzheimers+Dis
2018 ; 62
(3
): 1261-1276
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Alzheimer s Disease, Oligomers, and Inflammation
#MMPMID29562537
Forloni G
; Balducci C
J Alzheimers Dis
2018[]; 62
(3
): 1261-1276
PMID29562537
show ga
The production of soluble amyloid-? oligomers (A?Os) and the activation of
inflammation are two important early steps in the pathogenesis of Alzheimer's
disease (AD). The central role of oligomers as responsible for the neuronal
dysfunction associated with the clinical features has been extended to the other
protein misfolding disorders definable, on this basis, as oligomeropathies. In
AD, recent evidence indicates that the mechanism of inflammation as a consequence
of neurodegeneration must be assessed in favor of a more direct role of glial
activation in the alteration of synaptic function. Our own experimental models
demonstrate the efficacy of anti-inflammatory treatments in preventing the
cognitive deficits induced acutely by A?Os applied directly in the brain.
Moreover, some promising clinical tools are based on immunological activation
reducing the presence of cerebral A? deposits. However, the strategies based on
the control of inflammatory factors as well as the amyloid aggregation show poor
or non-therapeutic efficacy. Numerous studies have examined inflammatory factors
in biological fluids as possible markers of the neuroinflammation in AD. In some
cases, altered levels of cytokines or other inflammatory markers in cerebrospinal
fluid correlate with the severity of the disease. Here we propose, according to
the precision medicine principles, innovative therapeutic approaches to AD based
on the patient's inflammatory profile/state. The earlier intervention and a
multifactor approach are two other elements considered essential to improve the
chances of effective therapy in AD.
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