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Plasma homocysteine, a metabolite involved in key cellular methylation processes seems to be implicated in cognitive functions and cardiovascular health with its high levels representing a potential modifiable risk factor for Alzheimer's disease (AD) and other dementias.
If TNF influences cerebral blood flow (CBF) in humans, then the chronically high levels associated with active RA may be implicated in cognitive impairment.
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Aberrant memory consolidation has been implicated in cognitive models of PTSD, and sleep is believed to play a vital role in this process6,8.
However, only very recently the ilPFC, a region which has previously been implicated in cognitive control processes39,40,41, has been linked to goal-directed and habitual behavioral control13.
Oxidative stress has been implicated in cognitive decline as seen during normal aging and in sporadic Alzheimer's disease (AD).
Neuropathological alterations in these same regions have been implicated in cognitive impairments of AD patients at an early stage of the disease.
The hippocampus shows a high susceptibility to mTBI-induced damage due to its anatomical localization and has been implicated in cognitive and neurological impairments after mTBI.
Alterations in amyloid beta precursor protein (APP) have been implicated in cognitive decline in Alzheimer's disease (AD), which is accelerated in Down syndrome/Trisomy 21 (DS/TS21), likely due to the extra copy of the APP gene, located on chromosome 21.
In senescence-accelerated mouse, mitofilin is implicated in cognitive disorder associated with mitochondrial dysfunction (Wang et al. 2008).
Among different neurotransmitters, serotonergic alterations have been implicated in cognitive alterations, and low extracellular serotonin levels seem to be associated with impaired learning and memory consolidation (Ramos-Rodriguez et al., 2013).
D1-class receptors are implicated in cognitive deficits observed in schizophrenic patients [16], and may be related to a distinct cluster of 'negative' symptoms including social withdrawal [17], [18].
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