| |
AD |
PD |
ALS |
CTE |
| 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 |
