TL;DR: It is demonstrated that the 5XFAD mice develop a significant selective neuron loss in layer 5 of the cortex, leaving the overall neuron number of the total frontal cortex and hippocampus unaffected, which correlates with abundant spinal cord pathology.

TL;DR: Cortical thickness and volume collectively confirmed the vulnerability of the prefrontal cortex, whereas in other cortical regions, such as in the parietal cortex, thickness was the only measure sensitive to the pronounced age-related atrophy.

TL;DR: The results suggest that earlier in the disease, regions of the posterior default mode network start to disengage whereas regions within the anterior and ventral networks enhance their connectivity, however, as the disease progresses, connectivity within all systems eventually deteriorates.

TL;DR: Short-term conversion to AD is predicted by single marker models to a comparable degree as by multimarker models in amnestic MCI subjects.

TL;DR: Clinical relevant decreased FC within the default-mode network (DMN) in the precuneus and posterior cingulate cortex compared with controls was observed in Alzheimer's disease.

TL;DR: The average FA values of cerebral white matter (WM) reached peak at the age 32 ± 6 years in a large group (831) of healthy human subjects aged 11-90.

TL;DR: It is shown that 12 months of twice-weekly resistance training led to functional changes in 2 regions of cortex previously associated with response inhibition processes-the anterior portion of the left middle temporal gyrus and the left anterior insula extending into lateral orbital frontal cortex-in community-dwelling senior women.

TL;DR: It is shown that very low carbohydrate consumption, even in the short term, can improve memory function in older adults with increased risk for Alzheimer's disease and ketone levels were positively correlated with memory performance.

TL;DR: It is suggested that microglial Aβ phagocytosis results in Aβ redistribution rather than biophysical degradation in vivo and thereby provides mechanistic insight to the lack of amyloid burden elimination by parenchymal microglia in aged adults and those suffering from Alzheimer's disease.

TL;DR: By using a neuronal cell model of tauopathy, it is shown that activation of autophagy suppresses tau aggregation and eliminates cytotoxicity, and trehalose may be a good candidate for developing therapeutic strategies for AD and other tauopathies.

TL;DR: Multivariate analyses combining both methods of analysis by considering the activity of various parts of the DMN as well as the interconnectivity between these regions are required to achieve optimal and clinically acceptable diagnostic power.

TL;DR: Findings suggest that most DTI-derived changes in AD and a-MCI are largely secondary to gray matter atrophy, however, specific DR signal increases in posterior parts of the inferior fronto-occipital and longitudinal fasciculi may reflect early WM compromise in preclinical dementia, which is independent of atrophy.

TL;DR: The most common form of the disease, late onset Alzheimer's disease (LOAD), is a sporadic one presenting itself in later stages of life as mentioned in this paper, however, the genetic component has been the target of a large number of studies, because only one genetic risk factor (APOE4) has been consistently associated with the disease.

TL;DR: It is demonstrated that kaempferol, but not quercetin, myricetin or resveratrol, protects SH-SY5Y cells and primary neurons from rotenone toxicity, as a reduction of caspases cleavage and apoptotic nuclei are observed.

TL;DR: Education, occupation attainment, and leisure activities were found to contribute differently to reserve capacity and education could play a role in the constitution of cerebral reserve capacity.

TL;DR: It is demonstrated that structural brain changes occur years before clinical cognitive decline in AD and are localized to regions affected by AD neuropathology.

TL;DR: B baseline age differences in spatial strategies are established and a preference for allocentric strategy on the Y-maze strategy assessment was found to benefit performance on an independent assessment (virtual Morris water task) only in younger adults.

TL;DR: The results suggest that isoflurane may increase the levels of proinflammatory cytokines, which may cause neuroinflammation, leading to promotion of AD neuropathogenesis.

TL;DR: It is suggested that hUCB-MSC produced their sustained neuroprotective effect by inducing a feed-forward loop involving alternative activation of microglial neuroinflammation, thereby ameliorating disease pathophysiology and reversing the cognitive decline associated with Aβ deposition in AD mice.

TL;DR: The clinical and neuropathological features of 7 cases with PLA2G6 mutations clearly represent a link between PLA2 G6 and parkinsonian disorders.

TL;DR: Pterostilbene is a more potent modulator of cognition and cellular stress than resveratrol, likely driven by increased peroxisome proliferator-activated receptor alpha expression and increased lipophilicity due to substitution of hydroxy with methoxy group in pterostILbene.

TL;DR: Neopterin levels independently related to higher numbers of enlarged Virchow Robin spaces and an inflammatory process with activated monocytes/macrophages may play a role in the increased permeability of the blood brain barrier in patients with CSVD.

TL;DR: The results suggest that intermediate phenotypes, when coupled with larger sample sizes, may be a useful tool to dissect susceptibility loci for age-related cognitive decline and uncover shared molecular pathways with a role in neuronal injury.

TL;DR: An acute bout of moderate exercise improved Stroop performance in older adults, and this was associated with contralateral compensatory activation.

TL;DR: It is indicated that Al toxicity is mediated through ROS production and iron accumulation and a remedial route to reduce toxicity due to Al exposure is suggested and genetic and pharmacological efforts to reduce ROS or chelate excess Fe significantly mitigated Al toxicity.

TL;DR: The presence and susceptibility to aging of mitochondrial epigenetic mechanisms in the mammalian brain is demonstrated and TET immunoreactivity in the mitochondrial fraction is found.

TL;DR: The data reveal that AGEs can induce tau hyperphosphorylation and impair synapse and memory through RAGE-mediated GSK-3 activation and targeting RAGE/GSK-3 pathway can efficiently improve the AD-like histopathological changes and memory deterioration.

TL;DR: In vivo findings presented here demonstrate for the first time the therapeutic potential of P2X7R antagonism in the treatment of familiar Alzheimer's disease (FAD).

TL;DR: It is demonstrated that APP is a target of miR-16 and the abnormally low expression of mi R-16 could potentially lead to APP protein accumulation in AD mice.