Familial dementia means dementia that runs in a family. It happens because of changes in genes. These gene changes can be passed from a parent to a child. When a gene change is strong, a person can get dementia at a younger age than usual. This is sometimes called “early-onset.” Some familial dementias start in the 30s, 40s, or 50s.
Familial dementia means dementia that runs in families because of an inherited gene change. “Inherited” usually means autosomal dominant—a parent with the gene variant has a 50% chance to pass it to each child. In these families, symptoms often start younger than usual (sometimes before age 65) and several relatives across generations can be affected. Familiar examples include early-onset Alzheimer’s disease from changes in the APP, PSEN1, or PSEN2 genes; frontotemporal dementia (FTD) from MAPT, GRN, or C9orf72 changes; Lewy body–related or Parkinson’s-related dementias with certain gene variants; vascular familial dementias like CADASIL from NOTCH3; and rarer inherited conditions like genetic prion diseases (PRNP) and Huntington’s disease (HTT) where memory and thinking problems are part of a larger syndrome. Each of these conditions damages brain cells in different ways (amyloid plaques and tau tangles in Alzheimer’s; tau or TDP-43 protein problems in FTD; alpha-synuclein “Lewy bodies” in Lewy body disease; small-vessel injury in CADASIL; prion misfolding in PRNP; toxic huntingtin protein in Huntington’s), but the shared result is progressive decline in thinking, behavior, or language. Genetic testing and counseling help confirm a diagnosis and guide family planning. In autosomal dominant early-onset Alzheimer’s, every child of an affected parent has a one-in-two chance to inherit the pathogenic variant. NCBIPubMed CentralScienceDirect
There are different kinds of familial dementia. One kind is familial Alzheimer’s disease. It can be caused by gene changes in APP, PSEN1, or PSEN2. These gene changes are rare, but when they are present, they almost always cause Alzheimer’s disease in the person who carries them. This pattern is called autosomal dominant inheritance. That means each child has a 50% chance to inherit the gene change from an affected parent. National Institute on AgingNCBI
Another large group is genetic frontotemporal dementia (FTD). FTD affects behavior, language, or movement. About one in five people with FTD has a clear genetic cause. The three most common genes are C9orf72, GRN (progranulin), and MAPT (tau). The C9orf72 repeat expansion can also cause ALS (motor neuron disease), so the two conditions can occur in the same family. AFTD+1
Other familial dementias include genetic prion diseases (like familial Creutzfeldt-Jakob disease and fatal familial insomnia), and hereditary small-vessel diseases of the brain (like CADASIL, due to NOTCH3). These conditions have their own typical signs and test patterns. NCBI+1
Other names
People may also say:
Hereditary dementia
Genetic dementia
Familial Alzheimer’s disease (FAD)
Genetic FTD (C9orf72-, GRN-, or MAPT-related FTD)
Familial prion disease (familial CJD, GSS, or fatal familial insomnia)
Hereditary cerebral small-vessel disease (for CADASIL and related disorders)
Types
Familial Alzheimer’s disease (FAD). Most often due to APP, PSEN1, or PSEN2 variants. Onset is usually before age 65. Memory problems are early and strong. National Institute on Aging
Frontotemporal dementia (FTD) – genetic forms. Common genes are C9orf72, GRN, and MAPT. Main problems are behavior change, language loss, or movement symptoms. Age at onset can vary. AFTD
C9orf72 FTD/ALS spectrum. One repeat expansion can cause FTD, ALS, or both in a family. Each child of an affected person has a 50% chance to inherit the expansion. Penetrance can be age-dependent. NCBI
Genetic prion diseases. These include familial CJD, Gerstmann–Sträussler–Scheinker (GSS), and fatal familial insomnia (FFI). They often progress fast. They can cause dementia, movement jerks, and balance problems. NCBI
CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy). It is a hereditary small-vessel disease of the brain due to NOTCH3 changes. It causes strokes, migraines, mood change, and gradual thinking problems. NCBI+1
CARASIL and other rare small-vessel diseases. These are less common, but some are autosomal recessive (for example HTRA1-related).
Lewy body and Parkinson’s disease with dementia – familial forms. In some families, changes in genes like SNCA (alpha-synuclein) or GBA increase risk of dementia with Parkinsonism.
Huntington disease (HTT expansions). This is mainly a movement disorder, but it also causes dementia and behavior change.
Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) due to CSF1R variants. It causes white matter damage and cognitive decline.
Lysosomal or metabolic conditions with adult onset, such as Niemann–Pick type C, can look like dementia in some adults.
(Items 7–10 are rarer but important in a full list; they explain why genetics can be broad in young-onset or familial cases.)
Causes
APP gene variants. They change amyloid processing. Extra sticky amyloid builds up and harms brain cells. National Institute on Aging
PSEN1 gene variants. They change gamma-secretase. This increases toxic amyloid. National Institute on AgingPubMed Central
PSEN2 gene variants. Similar to PSEN1 but less common. National Institute on Aging
MAPT gene variants. They affect tau protein. Tau forms tangles and damages neurons. AFTD
GRN (progranulin) variants. They lower progranulin levels. Nerve cells lose support and die earlier. AFTD
C9orf72 repeat expansion. A long GGGGCC repeat causes toxic RNA and proteins. It can cause FTD, ALS, or both. AFTDPubMed
PRNP variants (prion protein). Misfolded prion protein spreads and kills brain cells. This causes familial CJD, GSS, or FFI. NCBI
NOTCH3 variants (CADASIL). Arteries in the brain get sick and narrow. Small strokes and white-matter damage add up and cause dementia. NCBI
HTRA1 variants (CARASIL). Another small-vessel disease with white-matter injury.
CSF1R variants (ALSP). White-matter disease damages connections needed for thinking.
SNCA variants (alpha-synuclein). They lead to Lewy body disease with dementia.
GBA variants. They raise risk for Parkinson’s disease dementia and Lewy body dementia.
HTT expansion (Huntington). A long CAG repeat damages neurons in the striatum and cortex.
Down syndrome (trisomy 21 or APP duplication). Extra APP increases amyloid and causes early Alzheimer-type dementia. National Institute on Aging
Niemann–Pick type C (NPC1/NPC2). Cholesterol trafficking fails. Neurons get sick and die.
Mitochondrial disorders (e.g., MELAS, POLG). Low energy harms brain networks for memory.
TREM2 or TYROBP variants (microglial function). Brain immune cells cannot clear waste well.
COL4A1/COL4A2 variants. Small-vessel disease with brain bleeds and cognitive decline.
APOE-ε4 inheritance in families. Not a direct cause, but a strong risk factor that can cluster in families with late-onset Alzheimer’s.
Multiple-hit families. Some families have more than one risk gene or strong vascular risks together (for example, hypertension plus a mild risk variant), which can make dementia appear “familial.”
Symptoms
Memory loss. The person forgets recent events. They repeat questions.
Trouble planning. Tasks feel harder. Bills and schedules get mixed up.
Word-finding problems. The person cannot find simple words or names.
Understanding problems. Following long sentences is hard.
Behavior change. The person becomes rude, impulsive, or very quiet.
Apathy. They lose interest in hobbies and friends.
Mood change. Depression or anxiety grows.
Judgment problems. Unsafe choices with money, driving, or cooking.
Visuospatial problems. Getting lost in known places; trouble parking or using stairs.
Hallucinations or delusions. Seeing things or holding fixed false beliefs.
Sleep problems. Acting out dreams; very vivid dreams; insomnia (especially in FFI). NCBI
Movement problems. Stiffness, slowness, tremor, or balance issues.
Speech or language loss. In FTD, speech may become short or empty, or the person may not understand words. AFTD
Jerks or seizures. In prion disease, myoclonus is common. NCBI
Rapid decline in some disorders. Prion disease can worsen quickly over months. NCBI
Diagnostic tests
A) Physical exam (bedside, with the clinician)
General neurologic exam. The doctor checks strength, reflexes, coordination, and sensation. This helps tell if there is stroke, Parkinsonism, or other signs that point to a specific familial pattern (like CADASIL strokes or FTD-related movement signs).
Mental status observation. The clinician watches how the person speaks, follows orders, and behaves in the room. They note attention, memory, and insight.
Gait and balance exam. Walking and turning are checked. A wide-based or shuffling gait can suggest certain types of dementia or small-vessel disease.
Eye movement exam and visual fields. Abnormal saccades or field loss can support a specific syndrome (for example, posterior cortical problems).
Sleep and autonomic review. The clinician asks about acting out dreams, fainting, bowel or bladder change, and sweating. These clues can point to Lewy body disease, FFI, or Parkinsonian syndromes. NCBI
B) Manual (bedside) cognitive tests
MMSE (Mini-Mental State Examination). A quick paper test for orientation, memory, language, and drawing. It gives a rough score of thinking.
MoCA (Montreal Cognitive Assessment). A sensitive screen for early problems in attention, memory, and planning. It can detect mild signs earlier than MMSE.
Clock-drawing test. The person draws a clock face and sets a time. It tests planning and visuospatial skills.
Verbal fluency tests. The person lists words by letter or category in one minute. It checks language and executive function.
Trail Making Test (A and B). Pencil-and-paper lines connect numbers (A) or numbers and letters (B). It checks attention and mental flexibility.
These bedside tools do not give a specific genetic diagnosis. But they show the domains that are weak (memory vs language vs planning). That pattern helps point toward Alzheimer’s, FTD, Lewy body disease, or vascular causes.
C) Lab and pathological tests
Basic blood tests. These include blood count, electrolytes, kidney and liver tests, thyroid (TSH), vitamin B12 and folate. These rule out treatable causes that can copy dementia signs.
Infection screens when needed. Tests for syphilis or HIV may be done in the right setting, because these infections can cause cognitive decline.
Genetic testing (targeted). If the family pattern and features fit, a clinician may order gene tests for APP, PSEN1, PSEN2 (Alzheimer’s), C9orf72, GRN, MAPT (FTD spectrum), PRNP (prion disease), NOTCH3 (CADASIL), and others as indicated. Pre- and post-test counseling is essential. In C9orf72 families, each child has a 50% chance to inherit the expansion. National Institute on AgingAFTDNCBI
CSF Alzheimer’s biomarkers (the AT(N) system). Doctors may test the fluid around the brain for Aβ42 (amyloid), phospho-tau (tau), and sometimes total tau or neurodegeneration markers. These tests help confirm Alzheimer biology in life. PubMed CentralBioMed Central
CSF prion markers. For rapidly progressive cases, CSF may be tested for 14-3-3, total tau, and RT-QuIC (a prion amplification assay). Positive results support prion disease. CDCWashington State Department of Health
Progranulin blood level. Low progranulin can point to GRN-related FTD and guide gene testing (done in some centers).
Skin biopsy for CADASIL. Under the electron microscope, the lab may see granular osmiophilic material (GOM) around small arteries. This supports CADASIL when gene testing is unclear or not available. Today, NOTCH3 sequencing is the main confirmation. NCBI
Brain tissue (pathology) in selected cases. A biopsy is rare and used only when needed to rule out other disease. Autopsy confirms the exact pathology after death. For prion disease, specialized centers analyze brain tissue when available. Texas Health Services
D) Electrodiagnostic tests
EEG (electroencephalogram). EEG can show typical “periodic sharp wave complexes” in prion disease and can detect seizures. In other dementias, EEG may be normal or only mildly slow. CDC
Polysomnography (sleep study). If there is dream-enacting behavior or severe insomnia, a sleep study helps. It can support REM sleep behavior disorder in Lewy body disease or severe sleep disruption in FFI. NCBI
E) Imaging tests (what pictures can show)
MRI brain. This is the main scan. It can show hippocampal shrinkage in Alzheimer’s disease, frontal or temporal lobe loss in FTD, white-matter disease and lacunar strokes in CADASIL, or diffusion-weighted bright signals in prion disease. NCBICDC
CT brain. This helps when MRI is not possible. It is less sensitive but can show atrophy or strokes.
FDG-PET. This scan shows low sugar use in certain brain areas. Patterns can support Alzheimer’s disease or FTD when the exam is unclear. (Part of the NIA-AA AT(N) “N” category.) PubMed Central
Amyloid PET and Tau PET. These scans can show amyloid plaques or tau tangles in living people. They support the biological diagnosis of Alzheimer’s disease. (They are the A and T parts of the AT(N) framework.) PubMed Central
Vascular imaging. MR angiography or special MRI sequences can show small-vessel disease patterns that fit CADASIL. Skin biopsy and NOTCH3 testing confirm it when needed. NCBI
Non-pharmacological treatments
**1) Aerobic exercise (150 minutes/week): brisk walking or cycling improves cardiovascular health, mood, and may slow functional decline; strong recommendation in dementia care. Mechanism: increased cerebral blood flow, neurotrophic factors. Benefits: better stamina, mood, daily function. PubMed
2) Resistance training (2–3 days/week): maintains muscle mass and balance; benefits everyday safety and mobility.
3) Balance & gait therapy: targeted physiotherapy reduces falls in parkinsonian or vascular gait disorders.
4) Task-specific ADL training (occupational therapy): step-by-step practice to preserve dressing, cooking, finances; adds environmental cues and adaptive tools.
5) Speech-language therapy: for FTD-language variants or hypophonia in Parkinson’s; focuses on word-finding, communication strategies, and safe swallowing.
6) Cognitive stimulation therapy (CST): small-group, themed activities twice a week improve quality of life and may offer modest cognition benefits. Mechanism: engages multiple cognitive domains; Benefits: enjoyment, social contact. Cochrane Library
7) Reminiscence therapy: photos, music, and life stories to trigger positive memories; reduces apathy and improves mood. PubMed Central
8) Music therapy: rhythmic entrainment helps agitation and apathy; personalized playlists calm distress. Benefits: better behavior, caregiver relief. PubMed Central
9) Bright-light therapy (morning): anchors the sleep-wake cycle; reduces sundowning in some people. Frontiers
10) Sleep hygiene + sleep apnea treatment: consistent sleep/wake and CPAP for apnea; better daytime thinking and mood.
11) Mindfulness-based stress reduction (for caregivers and patients with preserved insight): improves stress handling; benefit is strongest for caregivers’ mental health.
12) Cognitive-behavioral strategies for anxiety/depression: structured coping skills reduce distress and behavior outbursts.
13) Education modules for families (“what to expect, what to do”): structured teaching on communication, routines, wandering prevention, meds, and crisis plans—this consistently improves caregiver outcomes and delays placement. Alzheimer’s.gov
14) Safety-first environmental design: visual cues, removal of trip hazards, locks/alarms for exits, medication organizers; mechanism: reduce cognitive load and risk.
15) Caregiver skills training & respite planning: teaches de-escalation, bathing/dressing techniques, and sets up regular breaks; reduces burnout. Alzheimer’s.gov
16) Social engagement plans: scheduled visits, support groups, intergenerational activities; fights isolation (a modifiable risk factor). Hawai‘i Dementia Initiative
17) Hearing rehabilitation (testing + hearing aids): treating hearing loss likely lowers dementia risk and improves communication after onset; strong 2024-25 evidence. Benefits: less confusion, better conversations. The LancetHawai‘i Dementia Initiative
18) Vision care (glasses, cataract surgery when needed): reduces cognitive load and falls; untreated vision loss is now a recognized risk factor. The Guardian
19) Mediterranean/MIND-style eating pattern coaching: practical meal planning improves heart-brain health and aligns with risk-reduction evidence. PubMed
20) Routine & calendar orientation (whiteboards, large clocks): reduces anxiety by making the day predictable.
21) Wandering and driving safety program: ID bracelets, GPS, driving re-evaluation, and transition plan to stop driving safely.
22) Behavioral activation schedules: build pleasant activities into every day to reduce apathy and agitation.
23) Multi-sensory environments (e.g., Snoezelen): gentle sensory inputs to soothe agitation in advanced stages.
24) Fall-prevention home modifications: grab bars, nightlights, non-slip mats, shoe choice; essential for those with parkinsonism or vascular gait.
25) Advance care planning & legal/financial coaching: early planning reduces crises and respects preferences.
Note on “gene therapy”: For familial dementias, true gene therapies are still research-only (for example, AAV-progranulin for GRN-FTD and antisense oligonucleotides against MAPT are in trials). They are not approved for routine care; access is through clinical trials. NCBIAFTD
Drug treatments
Doses below are common U.S. label or guideline ranges for adults; prescribers personalize them based on age, kidney/liver function, drug interactions, and tolerability.
Alzheimer’s disease core therapies
Donepezil (acetylcholinesterase inhibitor)—Start 5 mg nightly; 10 mg daily after 4–6 weeks if tolerated; in moderate–severe AD, some use 23 mg once daily after at least 3 months on 10 mg. Purpose: memory/attention support and daily function. Mechanism: increases acetylcholine. Side effects: nausea, diarrhea, vivid dreams, bradycardia. FDA Access Data
Rivastigmine (acetylcholinesterase inhibitor)—Capsules 1.5 mg twice daily, titrate to 3–6 mg BID; or transdermal patch 4.6 mg/24 h → 9.5 mg/24 h. Purpose: cognition/behavior benefit; also approved for Parkinson’s disease dementia. Side effects: GI upset (less with patch), weight loss. Alzheimer’s AssociationNINDS
Galantamine (acetylcholinesterase inhibitor)—ER 8 mg each morning → 16–24 mg/day. Purpose/mechanism: similar to above; all cholinesterase inhibitors may modestly improve cognition. Side effects: GI upset, syncope risk in frail elders. ScienceDirect
Memantine (NMDA receptor antagonist)—10 mg twice daily (or ER 28 mg daily). Purpose: in moderate–severe AD, supports daily function and behavior; often combined with a cholinesterase inhibitor. Mechanism: dampens excitotoxicity. Side effects: dizziness, constipation, confusion (rare). FDA Access Data+1
Lecanemab (LEQEMBI; anti-amyloid mAb)—10 mg/kg IV every 2 weeks (maintenance schedules may vary per label updates), for mild cognitive impairment/mild AD with amyloid confirmed. Purpose: modestly slows clinical decline. Mechanism: clears soluble/fibrillar Aβ. Key risk: ARIA (brain swelling/bleeding); MRI monitoring required; APOE ε4 carriers have higher ARIA risk. Side effects: infusion reactions, headache. FDA Access Data
Donanemab (KISUNLA; anti-amyloid mAb)—label supports monthly IV infusions with titration; finite treatment may be possible once amyloid is cleared on PET. Purpose/mechanism: similar to lecanemab. Key risk: ARIA (boxed warning); MRI monitoring and careful symptom checks required; FDA approved July 2, 2024 with later dosing update July 2025 to mitigate ARIA. Side effects: infusion reactions, headache. ReutersFDA Access DataU.S. Food and Drug Administration
Important: Anti-amyloid therapies are for early Alzheimer’s with confirmed amyloid and require MRI monitoring and careful selection per updated PET AUC and FDA labeling. PubMed
Frontotemporal dementia (symptom-targeted; no disease-modifying drug yet)
Sertraline (SSRI)—50–200 mg daily. Purpose: reduce disinhibition, irritability, compulsions, depression/anxiety in FTD. Mechanism: serotonin reuptake inhibition. Side effects: GI upset, sleep change, hyponatremia (older adults). AFTD
Citalopram (SSRI)—10–20 mg daily (watch QTc at higher doses). Purpose/mechanism/benefits: as above. Side effects: QT prolongation risk, GI effects. AFTD
Trazodone (serotonergic antidepressant)—50–150 mg at night. Purpose: improves sleep and reduces agitation/anxiety in some FTD patients. Mechanism: 5-HT2 antagonism and antihistamine effects. Side effects: sedation, orthostasis. AFTD
Quetiapine (atypical antipsychotic; last-line, low dose)—12.5–50 mg at night, only if severe aggression/psychosis threaten safety and SSRIs fail. Purpose: short-term behavior control. Risks: stroke, mortality warning in dementia; metabolic effects; extrapyramidal symptoms—use sparingly. AFTD
Lewy body/Parkinson’s dementia
Rivastigmine (see above)—helps cognition and may lessen hallucinations. Caution: typical antipsychotics (e.g., haloperidol) can be dangerous in LBD; even atypicals require extreme caution. NINDSLewy Body Dementia Association
Pimavanserin (5-HT2A inverse agonist)—34 mg daily for Parkinson’s psychosis; sometimes used off-label in LBD when hallucinations are severe and other options fail. Risks: QT prolongation, boxed mortality warning for dementia psychosis (class). Use only with specialist oversight. PsychiatryOnline
Vascular familial dementia (e.g., CADASIL) and risk-factor meds
Blood-pressure control (ACE inhibitor/ARB, thiazide, etc.)—targets small-vessel injury; clinician chooses agent based on comorbidities. Purpose: stroke prevention and cognitive protection.
Antiplatelet therapy (after ischemic events; individualized in CADASIL due to microbleed risk). Purpose: reduce recurrent ischemic stroke risk; avoid agents with bleeding risk when hemorrhage risk is high. Discuss with stroke specialist. AHA Journals
Huntington’s disease cognition-behavior adjuncts
Deutetrabenazine or tetrabenazine (for chorea)—titrate to effect per label. Purpose: reduce involuntary movements that worsen function/safety. Mechanism: VMAT2 inhibition. Side effects: depression risk, parkinsonism, somnolence—specialist supervision is essential. NCBIPubMed
Dietary “molecular” supplements
Supplements are not cures; discuss with your clinician to avoid interactions. Evidence varies; diet patterns (Mediterranean/MIND) have stronger support than isolated pills. PubMed
Omega-3 (EPA+DHA): 1–2 g/day. Function: anti-inflammatory, vascular support. Mechanism: membrane fluidity, resolvins.
Vitamin D3: 800–2000 IU/day (per level). Function: bone, immune, mood support. Mechanism: nuclear receptor modulation.
Vitamin B12 (methylcobalamin): 1000 mcg/day (deficiency). Function: prevents neuropathy and reversible cognitive issues. Mechanism: one-carbon metabolism.
Folate: 400 mcg/day (diet/deficiency). Function: homocysteine lowering. Mechanism: methylation pathways.
Thiamine (B1): 50–100 mg/day (if risk factors). Function: energy metabolism.
Magnesium L-threonate: label-guided dosing (~1–2 g/day product; ~144 mg elemental Mg). Function: sleep/anxiety; limited cognition data.
Curcumin (enhanced-bioavailability): 500–1000 mg/day. Function: antioxidant; mixed human data.
Resveratrol: 100–500 mg/day. Function: antioxidant; limited clinical effect.
Phosphatidylserine: 100 mg three times daily. Function: membrane support; small trials suggest modest benefit.
Probiotic combo: labeled dose. Function: gut–brain axis; may help mood and bowel regularity.
Regenerative / stem-cell drugs”
There are no approved “immunity booster,” regenerative, or stem-cell drugs for familial dementias. What exists are research-only approaches:
Anti-amyloid monoclonals (lecanemab, donanemab)—approved for early AD (see above), not “immune boosters,” but they engage the immune system (microglial clearance) to remove amyloid; they require MRI monitoring due to ARIA. FDA Access Data+1
AAV-Progranulin gene therapy (for GRN-FTD)—aims to restore progranulin levels; clinical-trial only. Mechanism: gene replacement. Status: investigational. NCBI
MAPT antisense oligonucleotide (BIIB080)—reduces tau production; trial-stage only. Mechanism: RNA-targeting to lower tau. AFTD
Other ASOs/gene editing (C9orf72, APP/PSEN pathways)—preclinical/early clinical. Mechanism: silence toxic transcripts or correct mutations. Not approved.
Cell therapies (stem cells) for dementia—no robust evidence; not approved; avoid commercial “stem-cell” clinics making claims.
Neurotrophic or synaptic plasticity agents—various trial drugs (e.g., BDNF pathway modulators) remain experimental.
Procedures/surgeries
There is no surgery that cures dementia, but selected procedures can improve symptoms or safety:
Ventriculoperitoneal (VP) shunt—for normal pressure hydrocephalus (a different condition that can mimic dementia with gait and urinary symptoms). Why: improves gait/thinking when the cause is CSF buildup.
Carotid endarterectomy/stenting—in carefully selected patients with severe carotid stenosis and symptoms to lower stroke risk; protects brain health in vascular disease.
Deep brain stimulation (DBS)—for Parkinson’s tremor/rigidity in selected cases; not a dementia treatment, but better motor control can improve daily function.
Cataract surgery—improves vision; better sensory input can boost orientation and reduce falls; untreated vision loss is a risk factor. The Guardian
Cochlear implantation/hearing aids—for significant hearing loss; better hearing supports communication and may reduce cognitive decline risk. The Lancet
Preventions
Genetic counseling before/after testing; discuss predictive testing, reproductive options (including preimplantation genetic testing). NCBI
Treat hearing loss early (hearing aids). The Lancet
Control blood pressure from midlife onward. The Lancet
Do not smoke; get help to quit. The Lancet
Limit alcohol (avoid heavy use). Neurology live
Prevent/mitigate head injury (helmets, fall-proof homes). The Lancet
Exercise regularly (aerobic + strength). PubMed
Manage diabetes, cholesterol, and weight. The Lancet
Handle depression & social isolation (treatment and social plans). The Lancet
Follow Mediterranean/MIND-style eating and keep the brain engaged with education and cognitively stimulating activities across life. PubMed
The Lancet Commission (2024 update) highlights 14 modifiable risk factors (including hearing and vision) and estimates that addressing them could delay or prevent a large fraction of dementia cases. Hawai‘i Dementia Initiative
When to see doctors (red flags)
See a clinician urgently if you or a family member has:
• Rapid decline over weeks–months; new focal weakness, speech trouble, or vision loss (possible stroke or prion disease).
• Severe behavior change, dangerous wandering, delusions, or hallucinations—especially if on anticholinergic or dopamine-boosting drugs.
• New gait imbalance/falls, fainting, or repeated nighttime acting-out dreams (possible Lewy body spectrum).
• Early-onset symptoms (<65) plus strong family history (consider genetic evaluation).
• Head injury, loss of consciousness, or any new neurologic symptom. NINDS
What to eat” and “what to avoid
Eat more:
Leafy greens (spinach, kale) most days.
Berries several times/week.
Olive oil as main fat.
Whole grains (oats, brown rice).
Legumes (lentils/beans) often.
Fish (especially oily fish) 1–2×/week.
Nuts (small handful daily).
Colorful vegetables daily.
Low-fat fermented dairy (yogurt) if tolerated.
Plenty of water and regular meal timing. PubMed
Avoid or limit:
Processed meats and deep-fried foods.
Refined sugars/sweets and sugary drinks.
Excess salt (watch packaged foods).
Excess alcohol.
Very large evening meals that worsen sleep.
FAQs
1) What does “familial” really mean?
A strong inherited component—often autosomal dominant—with a 50% chance for each child to inherit the variant in conditions like APP/PSEN1/PSEN2 Alzheimer’s. NCBI
2) How is familial dementia confirmed?
By clinical pattern, imaging/biomarkers, and genetic testing with counseling when a familial syndrome is suspected. NCBI
3) Should every family member be tested?
No. Predictive genetic testing is optional and done with careful counseling to discuss benefits, risks, timing, and life planning. NCBI
4) Are there blood tests that diagnose Alzheimer’s?
Plasma biomarkers are emerging, but widely used, validated CSF and PET remain key in many settings; updated amyloid/tau PET AUC guide appropriate use. PubMed
5) What treatments slow Alzheimer’s in families with APP/PSEN1/PSEN2?
Cholinesterase inhibitors +/− memantine help symptoms; anti-amyloid antibodies (lecanemab, donanemab) modestly slow decline in early AD with amyloid confirmed and require MRI safety monitoring for ARIA. FDA Access Data+1
6) Do these antibody drugs work for FTD, CADASIL, or prion disease?
No—those are different diseases. Research is exploring gene-specific therapies for some forms of FTD. NCBI
7) Are antipsychotics safe in Lewy body dementia?
People with LBD can be extremely sensitive—typical antipsychotics can cause severe reactions; even atypicals require caution and specialist oversight. Lewy Body Dementia Association
8) Can lifestyle changes still help if the cause is genetic?
Yes. Managing hearing/vision, blood pressure, exercise, mood, sleep, and social connection supports function and may reduce additional decline burden. Hawai‘i Dementia Initiative
9) What about supplements?
Some are reasonable for deficiencies (B12, vitamin D) or general health (omega-3). None are cures. Discuss interactions with your clinician.
10) How do we plan for safety?
Create routines, simplify the home, ensure medication management, plan for driving retirement, and set up wandering safeguards early.
11) What legal/financial steps are smart to take early?
Advance directives, power of attorney, will, and long-term care plans—done while decision-making is strong.
12) Are there clinical trials for gene therapy?
Yes—for example, progranulin gene therapy for GRN-FTD and MAPT antisense—but these are trial-only. Ask a specialist about eligibility. NCBI
13) Is depression common?
Yes—treat it; depression itself is a modifiable risk factor for dementia and worsens quality of life if untreated. The Lancet
14) Can hearing aids really matter?
Growing evidence shows treating hearing loss reduces cognitive decline risk and improves day-to-day communication. The Lancet
15) Where do we start?
With a memory clinic or neurologist experienced in familial dementias, plus a genetic counselor. Build a care team early.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: September 01, 2025.
