Skip to main content

Table 1 Summary of neurocognition, neuroimaging, neuropathology, and pathophysiology of brain disturbances in HIV and Alzheimer’s disease

From: HIV effects on age-associated neurocognitive dysfunction: premature cognitive aging or neurodegenerative disease?

 

HIV

Alzheimer’s disease

Both

Neurocognitive manifestations

Psychomotor slowing

Primary amnestic disturbance

Memory disturbances

Executive dysfunction

Anomia

Selective cognitive impairments

Global cognitive dysfunction

Cerebral volumetric changes

Early declines in basal ganglia and frontal lobe volumes

Greater cortical atrophy and ventricular enlargement

Early white matter changes

DTI findings

Early frontal lobe changes

Early hippocampal changes

Globally decreased FA

MRS findings

Elevated Cho

 

Decreased NAA

Elevated MI

Aβ

Diffuse

Neuritic

Occur in neocortical areas

Extracellular and intracellular

Primarily extracellular

pTau

  

Elevated in medial temporal lobe

CSF markers

Inconsistent Tau findings

Elevated pTau

Decreased amyloid

ApoEε4

 

Robust relationship with cognitive dysfunction and dementia risk

Increases risk for Aβ, cerebral atrophy, cognitive dysfunction, and disease progression

BBB

  

Altered function

Glucose metabolism

Increased in basal ganglia

Decreased in parieto-temporal areas, posterior cingulate cortices, and medial temporal lobes

 

Decreased in frontal lobes

Mitochondrial function

  

Impaired

Neurotoxicity

  

Increased

Oxidative stress

  

Increased

Inflammation

  

Increased

Vascular and metabolic influences

May occur as a result of HIV

 

Exacerbate cognitive effects

Increase Aβ burden

  1. Findings common to both diseases are listed, along with findings unique to each. Aβ, beta-amyloid; ApoEε4, apolipoprotein-E ε4; BBB, blood–brain barrier; Cho, choline; CSF, cerebrospinal fluid; DTI, diffusion tensor imaging; FA, fractional anistropy; MI, myoinositol; MRS, magnetic resonance spectroscopy; NAA, N-acetylaspartate; pTau, hyperphosphorylated tau.