Clinical Manifestations
Patients may struggle to find/understand words during conversation due to this progressive neurocognitive disorder
Aphasia
Overactivation of NMDA receptors by excess glutamate leads to increased calcium influx into neurons, causing cellular damage and death
Excitotoxicity
Clinical assessment method that evaluates episodic memory, executive function, language, and visuospatial skills using standardized tools like the MMSE or MoCA
Neurocognitive testing
Monoclonal antibody therapy that binds aggregated beta-amyloid in the brain to slow progression of cognitive decline
Lecanemab therapy
The two proteins involved in abnormal protein folds: extracellular deposits of one protein and intracellular tangles of another
Beta-amyloid plaques and Tau tangles
This condition may cause agitation, paranoia, and mood changes as it gradually influences personality and behavior
Behavioral/personality changes
Extracellular buildup of misfolded protein forms plaques that interfere with neuron to neuron communication
Beta-amyloid plaques
Neuroimaging finding showing reduced glucose metabolism in the temporal and parietal lobes on PET scan
Temporoparietal hypometabolism
Drug class that increases acetylcholine levels by inhibiting the enzyme that breaks it down, commonly used to improve memory symptoms
Cholinesterase inhibitors
This neurotransmitter becomes deficient because neurons in the basal forebrain degenerate, contributing to memory problems
Acetylcholine
Individuals lose awareness of time and place even in familiar environments
Disorientation
Progressive loss of neurons and synapses, especially in memory related brain regions
Neurological degradation
Structural brain change seen on MRI characterized by shrinkage of the hippocampus and medial temporal lobe
Hippocampal atrophy
Medication that works as an NMDA receptor antagonist to reduce glutamate-induced excitotoxic neuronal damage in moderate to severe cases
Memantine therapy
Typically begin with short-term memory loss and progress to the loss of long-term memory, along with the inability to understand new information
Amnesia
Individuals require assistance with dressing, bathing, and other self-care activities
Loss of activities of daily living (ADLs)
Structural change occurs as brain tissue shrinks over time, particularly in the hippocampus and cortex
Cerebral atrophy
Cerebrospinal fluid biomarker pattern showing decreased beta-amyloid and increased tau protein levels
Abnormal CSF protein profile
Non-drug intervention that uses structured cognitive exercises and social engagement to help maintain thinking skills and daily functioning
Cognitive stimulation therapy
This lobe of the brain, important for forming memories, is commonly affected early
Temporal lobe
Difficulty remembering recent events while long-term memories remain intact early on
Short-term memory loss
Neurotransmitter system is reduced contributing to memory and learning deficiencies
Decreased acetylcholine
First-line diagnostic imaging modality used to rule out tumors, strokes, or other structural brain causes of memory loss in a patient with cognitive decline
Brain MRI
Treatment approach that focuses on improving daily functioning, safety, and quality of life through caregiver support, routines, and environmental modifications rather than curing disease
Supportive care management
After brain tissue dies, this is where the first real changes occur
Neurons