Dementia & Memory Disorders (Alzheimer’s disease, MCI)
Dementia, Alzheimer’s disease and Mild Cognitive Impairment (MCI): diagnosis, neurobiology and modern treatment options by psychiatrist Paschalis Gkikas in Athens.
Dementia & Memory Disorders (Alzheimer’s disease, MCI)
Dementia, Alzheimer’s disease and Mild Cognitive Impairment (MCI): diagnosis, neurobiology and modern treatment options by psychiatrist Paschalis Gkikas in Athens.
What is dementia?
Dementia is not a single disease — it is a syndrome: a set of symptoms reflecting progressive decline in cognitive functions to a degree that affects everyday autonomy. ICD-10 (F00–F09) describes the main clinical entities:
- Alzheimer’s disease (F00 / G30): The most common cause (~60–70%). It is characterized by β-amyloid deposition and tau neurofibrillary pathology, with progressive atrophy of hippocampal structures.
- Vascular dementia (F01): Ischemic lesions from strokes or chronic small-vessel disease — a “stepwise” deterioration rather than a gradual one.
- Dementia with Lewy bodies (F02.8): Visual hallucinations, parkinsonism and marked fluctuations in alertness as the classic triad.
- Frontotemporal dementia / FTD (F02.0): Personality changes and disinhibition at relatively younger ages — often misunderstood as a psychiatric problem without a cognitive substrate.
- Mild Cognitive Impairment / MCI (F06.7): The critical “intermediate” stage between normal aging and dementia — the window of intervention that can change the trajectory.
Clinical presentation & symptoms
Cognitive symptoms
- Difficulty recalling recent events, while older memories remain relatively preserved
- Repeated questions or stories within the same conversation
- Inability to learn new information
- Disorientation in time and place
- Difficulty with planning, financial transactions and complex tasks
Behavioral and psychiatric symptoms (BPSD)
- Depression, apathy, anxiety
- Aggression, agitation, agnosia
- Visual hallucinations, especially in Lewy body dementia
- Reversal of the sleep-wake cycle
- Delusional ideas, such as theft or infidelity
Functional symptoms
- Difficulty with self-care, such as dressing, cooking or taking medication
- Abandonment of hobbies and social isolation
- Increasing dependence on caregivers
Neurobiological basis
- Neurodegeneration: Progressive neuronal loss in the hippocampus, amygdala and prefrontal cortex.
- Proteinopathies: β-amyloid in Alzheimer’s disease, α-synuclein in Lewy body dementia, TDP-43 in FTD — each dementia subtype has its own molecular “signature”.
- Cholinergic dysfunction: Marked reduction in acetylcholine — the main neurotransmitter involved in memory consolidation.
- Neuroinflammation: Chronic microglial activation accelerates degeneration.
- Vascular factors: Hypertension, diabetes mellitus and hypercholesterolemia — modifiable risk factors with direct clinical relevance.
Treatment approach
Dementia management requires a multilayered approach. Psychiatrist Paschalis Gkikas coordinates the treatment plan in collaboration with neurologists and geriatric specialists when needed, with emphasis on personalization according to each patient’s clinical profile.
First-line treatments
- Cholinesterase inhibitors (donepezil, rivastigmine, galantamine): They enhance cholinergic transmission. They are indicated in mild-to-moderate Alzheimer’s disease and Lewy body dementia.
- Memantine: An NMDA receptor antagonist for moderate-to-severe Alzheimer’s disease — protects against glutamatergic neurotoxicity.
- PGx for BPSD: Psychiatric symptoms such as depression, agitation and psychosis are treated pharmacologically. Pharmacogenomic analysis allows safer medication selection in older adults with polypharmacy.
- Cognitive rehabilitation: Structured programs to maintain cognitive capacity.
Second-line & emerging treatments
- tDCS (transcranial direct current stimulation): Emerging non-invasive neuromodulation for cognitive enhancement in MCI and early dementia, with accumulating encouraging research data.
- rTMS: Protocols targeting hippocampal networks for cognitive enhancement in MCI are under investigation.
- Modification of vascular factors: Antihypertensive treatment, glucose regulation and anticoagulants in atrial fibrillation — especially important in vascular dementia.
In clinical practice, collaboration with the caregiver is as important as treatment of the patient. Education, psychological support and realistic planning are integral parts of every treatment plan.
Frequently asked questions (FAQ)
What is the difference between MCI and Alzheimer’s disease?
In MCI there is measurable cognitive decline on testing, but everyday autonomy remains almost intact. In Alzheimer’s disease, functioning is significantly affected. Approximately 10–15% of MCI cases progress to dementia each year — which makes early assessment decisive.
Is Alzheimer’s disease hereditary?
The vast majority (~95%) is “sporadic”, without strict hereditary transmission. However, the APOE ε4 genotype is an important risk factor. Genetic assessment is an option in selected cases.
Can sleep affect memory in the long term?
Yes. During sleep, the brain’s glymphatic system clears toxic protein residues, including β-amyloid. Chronic insomnia is associated with increased Alzheimer’s disease risk.
When should I see a psychiatrist for a memory problem?
When forgetfulness affects professional or daily responsibilities, when you repeat yourself in the same conversations, or when people close to you notice changes in your behavior or personality. Early assessment opens therapeutic windows.
