Clinical signs & symptoms Dementia;  progressive cognitive impairments memory loss -Motor symptoms resting tremor, rigidity, bradykinesia, impaired balance -Comorbid symptoms: depression, MCI, olfaction dysfunction -Progressive weakness, atrophy, and spasticity of muscle caused by motor neuron death -Affective disturbances; irritability, depression, aggression -Social instability, memory loss, cognitive decline -Motor impairments
Pathology/ Abnormal proteins -Aβ -Tau NFTs (uniformly distributed, less dense than CTE) -Dopaminergic lesions in substantia nigra (SN) -Lewy body accumulation, specifically a-synuclein -TDP 43 -Increased microglial activation - Aβ (less consistent that AD) -Tau NFTs (randomly distributed dense clusters, depths of sulci, superficial layers) -a-synuclein and TDP-43
Gross structural findings -Global atrophy -Increased VBR -Atrophy to hippocampus, amygdala,  & uncus -Regional atrophy in hippocampus, amygdala, orbitofrontal cortex, SN, & anterior cingulate -Trend of global cerebral atrophy -Global cerebral atrophy and various subcortical structures -Increased VBR -cavum septum pellucidum -septal fenestrations -thinning of CC -pallor of SN
Microstructural WM injuries -Global WM abnormalities.  Specifically uncinate, ILF, SLF, fornix, cingulum, hippocampus & CC -WM impairments in SN, CC, hippocampus, SLF, ILF, uncinate, cingulum, external capsule, corticospinal tract, & cerebellum -Marked damage to corticospinal tract -WM impairments in primary motor cortex, SMA, basal ganglia, precuneus, and CC -Unknown -Populations with frequent exposure to head trauma generally have damaged microstructural WM as a result of DAI
Functional abnormalities -Hyperactive DMN in early AD, but quickly diminishes as AD progresses -Hypometabolism throughout temporo-parietal cortex.  Specifically in the PCC, thalamus, hippocampus & frontal cortex -Neurochemical imbalance -disrupted connectivity in corticostriatal loops -increased FC in motor cortex and STN -increased CMRgl in STN, GP, motor cortex -Decreased CMRgl in prefrontal and inferior parietal regions -Impaired FC in sensorimotor, premotor, prefontral, and thalamic regions -Decreased FC between left and right primary motor cortices -Decreased DMN -Unknown -Populations with frequent exposure to head trauma reportedly exhibit decreased CMRgl in PCC, parieto-occipito lobes and cerebellum.  Altered FC in the DLPFC and frontal gyri are also reported in this population
Table 1: Features of NDs
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